Phenoxyphenylacetic acid derivatives

Abstract: Phenoxyphenylacetic acids and derivatives of the general structural formula I have endothelin antagonist activity and are useful in treating cardiovascular disorders, such as hypertension, postischemic renal failure, vasospasm, cerebral and cardiac ischemia, myocardial infarction, endotoxic shock, benign prostatic hyperplasia, inflammatory diseases including Raynaud's disease and asthma.

Description: This invention is concerned with non-peptidic endothelin receptor antagonists represented by the compound of Formula III, pharmaceutical compositions containing these compounds, as well as combination therapies which include a compound of the present invention. The compounds of the present invention are therapeutic agents particularly useful for the treatment of asthma, hypertension, pulmonary hypertension, arteriosclerosis, congestive heart failure, renal failure, particularly post-ischemic renal failure, cyclosporin nephrotoxicity, vasospasm, vascular restenosis, cerebral and cardiac ischemia and other ischemic states, myocardial infarction, Raynaud's disease, benign prostatic hyperplasia, inflammatory bowel diseases, including Crohn's disease and ulcerative colitis, as well as other inflammatory diseases, or endotoxic shock caused by or associated with endothelin. This invention further constitutes a method for antagonizing endothelin receptors in a mammal, including humans, which comprises administering to a mammal in need of such treatment an effective amount of a compound of Formula III. BACKGROUND OF THE INVENTION Endothelin is a 21-amino acid peptide produced by endothelial cells. The peptide is secreted not only by endothelial cells but also by tracheal epithelial cells or from kidney cells. Endothelin (ET-1) has a potent vasoconstrictor effect. The vasoconstricting effect is caused by the binding of endothelin to its receptor on the vascular smooth muscle cells. 1-3 Endothelin-1 (ET-1) is one of three recently identified potent vasoconstricting peptides which also includes endothelin-2 (ET-2) and endothelin-3 (ET-3) whose sequences differ from ET-1 by two and six amino acids, respectively. 4 Increased levels of endothelin are found in the blood of patients with essential hypertension, acute myocardial infarction, pulmonary hypertension, Raynaud's disease or atherosclerosis or in the washing fluids of the respiratory tract of patients with asthma compared to normal levels. 5-8 An experimental model of cerebral vasospasm and a second model of acute renal failure have led to the conclusion that endothelin is one of the mediators causing cerebral vasospasm following a subarachnoid hemorrhage, and renal failure. 9-10 Endothelin was also found to control the release of many physiological substances such as renin, atrial natriuretic peptide, endothelium-derived relaxing factor (EDRF), thromboxane A 2 , 14, prostacyclin, norepinephrine, angiotensin II and substance P. 11-16 Further, endothelin causes contraction of the smooth muscle of the gastrointestinal tract and the uterine smooth muscle. 17-19 Endothelin has also been shown to promote the growth of rat vascular smooth muscle cells which would suggest a possible relevance to arterial hypertrophy. 20 Endothelin receptors are present in high concentration in the peripheral tissues and also in the central nervous system, and cerebral administration of endothelin has been shown to induce behavioral changes in animals, suggesting that endothelin may play an important role in controlling neural functions. 21 Endotoxin has been shown to promote the release of endothelin. This finding has suggested that endothelin is an important mediator for endotoxin-induced diseases. 22-23 A study has shown that cyclosporin added to a renal cell culture- increased endothelin secretion. 24 Another study has shown that administration of cyclosporin to rats, led to a decrease in the glomerular filtration rate and an increase in the blood pressure, in association with a remarkable increase in the circulating endothelin level. This cyclosporin-induced renal failure can be suppressed by the administration of anti-endothelin antibody. 25 These studies suggest that endothelin is significantly involved in the pathogenesis of cyclosporin-induced renal disease. A recent study in patients with congestive heart failure demonstrated a good correlation between the elevated levels of endothelin in the plasma and the severity of the disease. 26 Endothelin is an endogenous substance which directly or indirectly (through the controlled release of various other endogenous substances) induces sustained contraction of vascular or non-vascular smooth muscles. Its excess production or excess secretion is believed to be one of the factors responsible for hypertension, pulmonary hypertension, Raynaud's disease, bronchial asthma, acute renal failure, myocardial infarction, angina pectoris, arteriosclerosis, cerebral vasospasm and cerebral infarction. See A. M. Doherty, Endothelin: A New Challenge , J. Med. Chem., 35 , 1493-1508 (1992). Substances which specifically inhibit the binding of endothelin to its receptor are believed to block the physiological effects of endothelin and are useful in treating patients with endothelin related disorders. The novel compounds of the present invention are useful as a non-peptidic endothelin antagonists, and have not been disclosed in any issued patents or published patent applications. Among the published patent applications disclosing linear and cyclic peptidic compounds as endothelin antagonists are the following: Fujisawa in European Patent Application EP-457,195 and Patent Cooperation Treaty (PCT) International Application No. WO 93/10144, Banyu in EP-436,189 and 460,679, Immunopharmaceutics Inc. in WO 93/225580, Warner Lambert Co. WO 92/20706 and Takeda Chemical Ind. in EP-528,312, EP-543,425, EP-547,317 and WO 91/13089 . Fujisawa has also disclosed two nonpeptidic endothelin antagonist compounds: anthraquinone derivatives produced by a fermentation process using Streptomyces sp. No. 89009 in EP-405,421 and U.S. Patent No. 5,187,195; and a 4-phenoxyphenol derivative produced by a fermentation process using Penicillium citreonigrum F-12880 in a UK Patent Application GB 2259450. Shionogi and Co. has also disclosed nonpepfidic endothelin antagonist triterpene compounds which were produced by a fermentation process using Myrica cerifera in WO 92/12991. Among the non-peptidic endothelin antagonist compounds which are known in the patent literature are: 1) a series of substituted (1,4-quinolinoxy)methylbiphenylcarboxylic acids disclosed by Roussel-Uclaf in EP-498,723; 2) a series of of N-(4-pyrimidinyl)benzenesulfonamides with different substitution patterns from Hoffmann-La Roche published in EP-510,526 and EP-526,708; 3) a series of naphthalenesulfonamides and benzenesulfonamides disclosed by E.R. Squibb & Sons in EP-558,258 and EP-569,193, respectively; 4) a series of compounds represented by 3-(3-indolylmethyl)-1,4-diaza-2,5-dioxobicyclo[4.3.0]nonane-9-carboxylic acid from Immunopharmaceutics Inc. in WO 93/23404; 5) a series of fused [1,2,4]thiadiazole substituted with an iminosulfonyl substituent from Takeda Chemical Ind. has been disclosed in EP-562, 599; and 6) a series of indane and indene derivatives from Smith-Kline Beecham Corp. disclosed in WO 93/08779. REFERENCES 1 Nature, 332 , 411-415 (1988). 2 FEBS Letters, 231 , 440-444 (1988). 3 Biochem. Biophys. Res. Commun. 154 , 868-875 (1988). 4 TiPS, 13 , 103-108, March 1992. 5 Japan J. Hypertension 12 , 79 (1989). 6 J. Vascular Medicine Biology, 2 , 207 (1990). 7 J. Am. Med. Association, 264 , 2868 (1990). 8 The Lancet, ii, 207 (1990) and The Lancet, ii, 747-748 (1989). 9 Japan. Soc. Cereb. Blood Flow & Metabol. 1 , 73 (1989). 10 J. Clin. Invest., 83 , 1762-1767 (1989). 11 Biochem. Biophys. Res. Comm. 157 , 1164-1168 (1988). 12 Biochem. Biophys. Res. Comm. 155 , 167-172 (1989). 13 Proc. Natl. Acad. Sci. USA, 85 , 9797-9800 (1989). 14 J. Cardiovasc. Pharmacol., 13 , 589-592 (1989). 15 Japan. J. Hypertension 12 , 76 (1989). 16 Neuroscience Letters, 102 , 179-184 (1989). 17 FEBS Letters, 247 , 337-340 (1989). 18 Eur. J. Pharmacol. 154 , 227-228 (1988). 19 Biochem. Biophys. Res. Commun., 159 , 317-323 (1989). 20 Atherosclerosis, 78 , 225-228 (1989). 21 Neuroscience Letters, 97 , 276-279 (1989). 22 Biochem. Biophys. Res. Commun. 161 , 1220-1227 (1989). 23 Acta. Physiol. Scand., 137 , 317-318 (1989). 24 Eur. J. Pharmacol., 180 , 191-192 (1990). 25 Kidney Int. 37 , 1487-1491 (1990). 26 Mayo Clinic Proc., 67 , 719-724 (1992). The present invention provides a compound of Formula III: or a pharmaceutically acceptable salt thereof, wherein: R 3a and R 3b are independently: (a) H, (b) F, Cl, Br, or I, (c) -NO 2 , (d) (C 1 -C 6 )-alkyl, (e) -OR 7 , (f) -NHCO-(C 1 -C 4 )-alkyl, (g) -NHCO-O(C 1 -C 4 )-alkyl, (h) -O-(CH 2 )m-OR 7 , (i) -CONR 7 R 11 , or (j) -COOR 7 ; R 1 and R 2 on adjacent carbon atoms are joined together to form a ring structure: A represents: a) -Y-[C(R 6 )(R 6 )] S -Y-, or b) -C(R 4 )=C(R 5 )-C(R 4 )=C(R 5 )-; m is 2, 3 or 4, n is 0, 1 or 2, s is 1 or 2, Y is -O-, -S- and NR 7 R 4 and R 5 are independently: (a) H, (b) (C 1 -C 6 )-alkyl, (c) (C 3 -C 7 )-cycloalkyl, (d) F, Cl, Br, I, (e) -NR 7 COOR 11 , (f) -SO 2 NR 7 R 11 , (g) -O-(C 1 -C 4 )-alkyl, (h) -S(O) n -(C 1 -C 4 )-alkyl, or (i) -NHSO 2 R 11 ; R 6 is: (a) H, or (b) (C 1 -C 4 )-alkyl; R 7 is: (a) H, (b) (C 1 -C 6 )-alkyl, (c) phenyl, or (d) benzyl; R 9 and R 10 are independently: (a) H, (b) (C 1 -C 6 )-alkyl, unsubstituted or substituted with (C 3 -C 7 )-cycloalkyl, (c) Cl, Br, F, I, (d) (C 1 -C 6 )-alkoxy, or (e) hydroxy-(C 1 -C 6 )-alkyl; R 11 is (a) (C 1 -C 6 )-alkyl, unsubstituted or substituted with a substituent selected from the group consisting of: i) -OR 7 , ii) -N[R 7 ] 2 , iii) -NH 2 , iv) -COOR 7 , or v) -N[CH 2 CH 2 ] 2 Q; (b) aryl, wherein aryl is defined as phenyl or naphthyl which is unsubstituted or substituted with one or two substituents selected from the group consisting of: i) (C 1 -C 4 )-alkyl, ii) -O-(C 1 -C 4 )-alkyl, iii) -CO[NR 7 ] 2 , iv) F, Cl, Br or I, v) -COOR 7 , vi) -NH 2 , vii) -NH[(C 1 -C 4 )-alkyl], viii) -N[(C 1 -C 4 )-alkyl] 2 , or ix) -CON[CH 2 CH 2 ] 2 Q; (c) -(C 1 -C 4 )-alkylaryl, wherein aryl is as defined above, (d) (C 3 -C 7 )-cycloalkyl, (e) R 7 and R 11 on the same nitrogen atom they can join together to form a ring selected from the group consisting of: morpholinyl, piperazinyl, or pyrrolyl, or Q is O, S or -NR 7 ; R 12 is (a) H, (b) (C 1 -C 6 )-alkyl, wherein alkyl is defined as unsubstituted or substituted with one or two substituents selected from the group consisting of: i) -OH, ii) -O-(C 1 -C 4 )-alkyl, iii) -O-(C 1 -C 4 )-cycloalkyl, iv) -S(O) n -(C 1 -C 4 )-alkyl, iv) -NR 7 -(C 1 -C 4 )-alkyl, v) -NR 7 R 11 , vi) -COOR 7 , vii) -CONHR 7 , viii) -OCOR 11 , ix) -CONR 7 R 11 , x) -NR 7 CONR 7 R 11 , xi) -NR 7 COOR 11 , xii) -C(R 6 )(OH)-C(R 6 )(R 7 )(OH), or xiii) -SO 2 NR 7 R 11 , (c) -COOR 7 , (d) -CONH 2 , (e) -CONR 7 R 11 , (f) -CONR 7 CO 2 R 7 , (g) -C(R 6 )(OH)-C(R 6 )(R 7 )(OH), or (h) -CONHSO 2 R 11 , (i) -SO 2 NR 7 R 11 , (j) -NR 7 SO 2 NR 7 R 11 , (k) -CO-amino acid, wherein amino acid is defined as an L-or D- amino acid selected from the group consisting of Ala, Ile, Phe, Asp, Pro and Val and which can be further substituted as a (C 1 -C 6 )-alkyl ester or an amide, or (l) X is -O-; Z is: (a) -CO 2 H, (b) -CO 2 R 13 , (c) -CONH-(tetrazol-5-yl), (d) -CONHSO 2 -aryl, wherein aryl is defined as phenyl or naphthyl which is unsubstituted or substituted with one or two substituents selected from the group consisting of: i) (C 1 -C 4 )-alkyl, ii) -O-(C 1 -C 4 )-alkyl, iii) -CONR 7 R 11 , iv) F, Cl, Br or I, v) -COOR 7 , vi) -NH 2 , vii) -NH[(C 1 -C 4 )-alkyl], viii) -N[(C 1 -C 4 )-alkyl] 2 , ix) -phenyl; (e) -CONHSO 2 -(C 1 -C 8 )-alkyl, wherein alkyl is unsubstituted or substituted as defined in R 4 (b), (f) -CONHSO 2 -heteroaryl, wherein heteroaryl is defined as carbazolyl, furyl, thienyl, pyrrolyl, isothiazolyl, imidazolyl, isoxazolyl, thiazolyl, oxazolyl, pyrazolyl, pyrazinyl, pyridyl, pyrimidyl, purinyl, or quinolinyl, which is unsubstituted or substituted with one or two substituents selected from the group consisting of: i) (C 1 -C 4 )-alkyl, ii) -O-(C 1 -C 4 )-alkyl, iii) -CONR 7 R 11 , iv) F, Cl, Br or I, v) -COOR 7 , vi) -NR 7 CONR 7 R 11 , and vii) -NR 7 COOR 11 ; (g) -tetrazol-5-yl; and R 13 is: (C 1 -C 4 )-alkyl. A subclass of the compounds of Formula III are the compounds of Formula IV: or a pharmaceutically acceptable salt thereof, wherein: R 1 and R 2 taken together form the ring structure: A represents: a) -Y-[C(R 6 )(R 6 )] S -Y-, or b) -C(R 4 )=C(R 5 )-C(R 4 )=C(R 5 )-; s is 1 or 2; Y is -O-; R 3a is: (a) H, (b) F, Cl, Br, or I, (c) (C 1 -C 6 )-alkyl, (d) -OR 7 , (e) -O-(CH 2 )m-OR 7 , (f) -CONR 7 R 11 , or (g) -COOR 7 ; m is 2, 3 or 4; R 4 and R 5 are independently: (a) H, (b) (C 1 -C 6 )-alkyl, (c) (C 3 -C 7 )-cycloalkyl, (d) F, Cl, Br, I, (e) -NR 7 COOR 11 , (f) -SO 2 NR 7 R 11 , (g) -O-(C 1 -C 4 )-alkyl, (h) -S(O) n -(C 1 -C 4 )-alkyl, or (i) -NHSO 2 R 11 ; n is 0, 1 or 2, R 6 is: (a) H, or (b) (C 1 -C 4 )-alkyl; R 7 is: (a) H, (b) (C 1 -C 6 )-alkyl, (c) phenyl, or (d) benzyl; R 9 is: (a) H, (b) (C 1 -C 6 )-alkyl, unsubstituted or substituted with (C 3 -C 7 )-cycloalkyl, (c) Cl, Br, F, I, (d) (C 1 -C 6 )-alkoxy, or (e) hydroxy-(C 1 -C 6 )-alkyl; R 11 is (a) (C 1 -C 6 )-alkyl, unsubstituted or substituted with a substituent selected from the group consisting of: i) -OR 7 , ii) -N[R 7 ] 2 , iii) -NH 2 , iv) -COOR 7 , or v) -N[CH 2 CH 2 ] 2 Q; (b) aryl, wherein aryl is defined as phenyl or naphthyl which is unsubstituted or substituted with one or two substituents selected from the group consisting of: i) (C 1 -C 4 )-alkyl, ii) -O-(C 1 -C 4 )-alkyl, iii) -CO[NR 7 ] 2 , iv) F, Cl, Br or I, v) -COOR 7 , vi) -NH 2 , vii) -NH[(C 1 -C 4 )-alkyl], viii) -N[(C 1 -C 4 )-alkyl] 2 , or ix) -CON[CH 2 CH 2 ] 2 Q; (c) -(C 1 -C 4 )-alkylaryl, wherein aryl is as defined above, (d) (C 3 -C 7 )-cycloalkyl, (e) R 7 and R 11 on the same nitrogen atom they can join together to form a ring selected from the group consisting of: morpholinyl, piperazinyl, or pyrrolyl, or Q is O, S or -NR 7 ; R 12 is (a) H, (b) (C 1 -C 6 )-alkyl, wherein alkyl is defined as unsubstituted or substituted with one or two substituents selected from the group consisting of: i) -OH, ii) -O-(C 1 -C 4 )-alkyl, iii) -O-(C 1 -C 4 )-cycloalkyl, iv) -S(O) n -(C 1 -C 4 )-alkyl, iv) -NR 7 -(C 1 -C 4 )-alkyl, v) -NR 7 R 11 , vi) -COOR 7 , vii) -CONHR 7 , viii) -OCOR 11 , ix) -CONR 7 R 11 , x) -NR 7 CONR 7 R 11 , xi) -NR 7 COOR 11 , xii) -C(R 6 )(OH)-C(R 6 )(R 7 )(OH), or xiii) -SO 2 NR 7 R 11 , (c) -COOR 7 , (d) -CONH 2 , (e) -CONR 7 R 11 , (f) -CONR 7 CO 2 R 7 , (g) -C(R 6 )(OH)-C(R 6 )(R 7 )(OH), or (h) -CONHSO 2 R 11 , (i) -SO 2 NR 7 R 11 , (j) -NR 7 SO 2 NR 7 R 11 , (k) -CO-amino acid, wherein amino acid is defined as an L-or D- amino acid selected from the group consisting of Ala, Ile, Phe, Asp, Pro and Val and which can be further substituted as a (C 1 -C 6 )-alkyl ester or an amide, or (l) X is -O-; Z is: (a) -CO 2 H, (b) -CO 2 R 13 , (c) -CONH-(tetrazol-5-yl), (d) -CONHSO 2 -aryl, wherein aryl is defined as phenyl or naplithyl which is unsubstituted or substituted with one or two substituents selected from the group consisting of: i) (C 1 -C 4 )-alkyl, ii) -O-(C 1 -C 4 )-alkyl, iii) -CONR 7 R 11 , iv) F, Cl, Br or I, v) -COOR 7 , vi) -NH 2 , vii) -NH[(C 1 -C 4 )-alkyl], viii) -N[(C 1 -C 4 )-alkyl] 2 , ix) -phenyl; (e) -CONHSO 2 -(C 1 -C 8 )-alkyl, wherein alkyl is unsubstituted or substituted as defined in R 4 (b), (f) -CONHSO 2 -heteroaryl, wherein heteroaryl is defined as carbazolyl, furyl, thienyl, pyrrolyl, isothiazolyl, imidazolyl, isoxazolyl, thiazolyl, oxazolyl, pyrazolyl, pyrazinyl, pyridyl, pyrimidyl, purinyl, or quinolinyl, which is unsubstituted or substituted with one or two substituents selected from the group consisting of: i) (C 1 -C 4 )-alkyl, ii) -O-(C 1 -C 4 )-alkyl, iii) -CONR 7 R 11 , iv) F, Cl, Br or I, v) -COOR 7 , vi) -NR 7 CONR 7 R 11 , and vii) -NR 7 COOR 11 , or (g) -tetrazol-5-yl; and R 13 is: (C 1 -C 4 )-alkyl. An embodiment of the compounds according to the present invention are: 2-[(2,6-dipropyl-4-hydroxymethyl)phenoxy]-2-(3,4-ethylenedioxyphenyl)acetic acid; 2-[(2,6-dipropyl-4-hydroxymethyl)phenoxy]-2-(3,4-methylenedioxyphenyl)acetic acid; 2-[(2,6-dipropyl-4-hydroxymethyl)phenoxy]-2-(2-naphthyl)acetic acid; 2-[(2,6-dipropyl-4-(2-hydroxyethyl)phenoxy]-2-(2-naphthyl)acetic acid; 2-[(2,6-dipropyl-4-(2-hydroxyethyl)phenoxyl]-2-(3,4-methylenedioxyphenyl)acetic acid; 2-[(2,6-dipropyl-4(1,2-dihydroxyethyl)phenoxy)]-2-(2-naphthyl)acetic acid; 2-[(2,6-dipropyl-4-(1-hydroxypentyl)phenoxy]-2-(2-naphthyl)acetic acid; 2-[(4-carboxy-2,6-dipropyl)phenoxy]-2-[3,4-methylenedioxyphenyl] acetic acid; (N-4-t-butylbenzenesulfonyl)-2-(4-methoxycarbonyl-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(benzenesulfonyl)-2-(4-methoxycarbonyl-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(4-phenylbenzenesulfonyl)-2-(4-methoxycarbonyl-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(4-chlorobenzenesulfonyl)-2-(4-methoxycarbonyl-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(4-methylbenzenesulfonyl)-2-(4-methoxycarbonyl-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(5-iso-butylthien-2-ylsulfonyl)-2-(4-methoxycarbonyl-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(4-methoxybenzenesulfonyl)-2-(4-methoxycarbonyl-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(4-dimethylaminobenzenesulfonyl)-2-(4-methoxycarbonyl-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(2-methylbenzenesulfonyl)-2-(4-methoxycarbonyl-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(2-methoxycarbonylbenzenesulfonyl)-2-(4-methoxycarbonyl-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(2-chlorobenzenesulfonyl)-2-(4-methoxycarbonyl-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(3-chlorobenzenesulfonyl)-2-(4-methoxycarbonyl-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(dansylsulfonyl)-2-(4-methoxycarbonyl-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(8-quinolinesulfonyl)-2-(4-methoxycarbonyl-2-propylphenoxy)-2-(3,4-methylenedioxyphenylacetamide; N-(4-t-butylbenzenesulfonyl)-2-(4-carboxy-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(benzenesulfonyl)-2-(4-carboxy-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(4-phenylbenzenesulfonyl)-2-(4-carboxy-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(4-chlorobenzenesulfonyl)-2-(4-carboxy-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(4-methylbenzenesulfonyl)-2-(4-carboxy-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(5-isobutylthien-2-ylsulfonyl)-2-(4-carboxy-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(4-methoxybenzenesulfonyl)-2-(4-carboxy-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(4-dimethylaminobenzenesulfonyl)-2-(4-carboxy-2-propylphenoxy)-3,4-methylenedioxyphenyl)acetamide; N-(2-methylbenzenesulfonyl)-2-(4-carboxy-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(2-methoxycarbonylbenzenesulfonyl)-2-(4-carboxy-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(2-chlorobenzenesulfonyl)-2-(4-carboxy-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(3-chlorobenzenesulfonyl)-2-(4-carboxy-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(dansylsulfonyl)-2-(4-carboxy-2-propylphenoxy)-3,4-methylenedioxyphenyl)acetamide; N-(8-quinolinesulfonyl)-2-(4-carboxy-2-propylphenoxy)-2-(3,4-methylenedioxyphenylacetamide; N-(8-quinolinesulfonyl)-2-(4-carboxamido-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; α-(4-carbomethoxy-2- n -propylphenoxy)-3,4-methylenedioxyphenylacetic acid; N -(4- iso -propylbenzenesulfonyl)-α-(4-carbomethoxy-2- n -propylphenoxy)-3,4-methylenedioxyphenylacetamide; N -(4- iso -propylbenzenesulfonyl)-α-(4-carboxy-2- n -propylphenoxy)-3,4-methylenedioxyphenylacetamide dipotassium salt; α-(2- iso -butyl-4-carbomethoxyphenoxy)-3,4-methylenedioxyphenylacetic acid; N -(4- iso -propylbenzenesulfonyl)-α-(2- iso -butyl-4-carbomethoxyphenoxy)-3,4-methylenedioxyphenylacetamide; N -(4- iso -propylbenzenesulfonyl)-α-(2- iso -butyl-4-carboxyphenoxy)-3,4-methylenedioxyphenylacetamide; N -(4- iso -propylbenzenesulfonyl)-α-(2- n -propyl-4-carboxamidophenoxy)-3,4-methylenedioxyphenylacetamide; N -(4- iso -propylbenzenesulfonyl)-α-(2- n -propyl-4-hydroxymethylphenoxy)-3,4-methylenedioxyphenylacetamide; α-(2- n -propylphenoxy)-3,4-methylenedioxyphenylacetic acid N -(4- iso -propylbenzenesulfonyl)-α-(2- n -propylphenoxy)-3,4-methylenedioxyphenylacetamide; α-(2-(2-hydroxyethyl)phenoxy)-3,4-methylenedioxyphenylacetic acid; α-(4-hydroxymethyl-2- n -propylphenoxy)-3,4-methylenedioxyphenylacetic acid; α-(4-(2-hydroxyethyl)-2- n -propylphenoxy)-3,4-methylenedioxyphenylacetic acid; N -(4- iso -propylbenzenesulfonyl)-2-(4-carbomethoxy-2- n -propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide; N-(4- iso -propylbenzenesulfonyl)-2-(4-carboxy-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide; N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-(4- iso -propylbenzenesulfonyl)carboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide; N-(4- iso -propylbenzenesulfonyl)-2-(4-carboxamido-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide; N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-methylcarboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide; N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-2-hydroxyethylcarboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide; N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-morpholinylcarboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide; N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-3-methylbutylcarboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide; N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-carboxymethylcarboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide; N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-(L-Ala-OEt)carboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide; N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-2-ethoxycarbonylethylcarboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide; N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-(L-Ala)carboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide; N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-2-carboxyethylcarboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide; N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-3-hydroxypropylcarboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide; N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-tetrazol-5-ylcarboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide; N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-3-(morpholin-4-yl)propylcarboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide; N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-(D-Ala-OMe)carboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide; N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-(D-Ala)carboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide; N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-(3-carboxymethylpropyl)carboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide; N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-(3-carboxypropyl)carboxamido)-2- n -propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide; α-(2- n -propyl-4-methylaminosulfonylphenoxy)-3,4-methylenedioxyphenylacetic acid; N -(4- iso -propylbenzenesulfonyl)-α-(2- n -propyl-4-methylamino-sulfonylphenoxy)-3,4-methylenedioxyphenylacetamide potassium salt. A perferred embodiment of the compounds of this invention are: N -(4- iso -propylbenzenesulfonyl)-α-(4-carboxy-2- n -propylphenoxy)-3,4-methylenedioxyphenylacetamide dipotassium salt; N-(8-quinolinesulfonyl)-2-(4-carboxy-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(4-dimethylaminobenzenesulfonyl)-2-(4-carboxy-2- n -propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide. The alkyl substituents recited above denote straight and branched chain hydrocarbons of the length specified such as methyl, ethyl, isopropyl, isobutyl, neopentyl, isopentyl, etc. The alkenyl-substituents denote alkyl groups as described above which are modified so that each contains a carbon to carbon double bond such as vinyl, allyl and 2-butenyl. Cycloalkyl denotes rings composed of 3 to 8 methylene groups, each of which may be substituted or unsubstituted with other hydrocarbon substituents, and include for example cyclopropyl, cyclopentyl, cyclohexyl and 4-metylcyclohexyl. The alkoxy substituent represents an alkyl group as described above attached through an oxygen bridge. The heteroaryl is defined as carbazolyl, furyl, thienyl, pyrrolyl, isothiazolyl, imidazolyl, isoxazolyl, thiazolyl, oxazolyl, pyrazolyl, pyrazinyl, pyridyl, pyrimidyl, purinyl or quinolinyl. Although the reaction schemes described below are reasonably general, it will be understood by those skilled in the art of organic synthesis that one or more functional groups present in a given compound of Formula III may render the molecule incompatible with a particular synthetic sequence. In such a case an alternative synthetic route, an altered order of steps, or a strategy of protection and deprotection may be employed. In all cases the particular reaction conditions, including reagents, solvent, temperature and time, should be chosen so that they are consistent with the nature of the functionality present in the molecule. The compounds of Formula III can be synthesized using the reactions and techniques described for the synthesis of the non-heterocyclic components in the patent application WO91/11999 (Merck & Co.; published on August 22,1991 under the Patent Cooperation Treaty) and also US Patent 5,177,095 (Merck & Co.; January 5, 1993). The reaction schemes described below have been generalized for simplicity. It is further to be understood that in the generalized schemes below, unless specified more narrowly in the text, the alkyl and aryl groups represent unfunctionalized or functionalized derivatives as described before. The leaving group Q present in the alkylating agents is either chloro, bromo, iodo, methanesulfonate, p-toluenesulfonate or triflate. More specifically, the compounds of Formula III can be synthesized as outlined in Scheme 1 . The substituted compound 1 may be reacted with the alkylating agent 2 in an appropriate solvent such as alcohols (methanol, ethanol, isopropanol and like), dimethylformamide (DMF), dimethylsulfoxide (DMSO), tetrahydrofuran (THF) and acetone in the presence of an alkali metal salt such as alkoxides, carbonates, hydroxides and hydrides, or organic bases such as trialkylamines or alkyl lithiums to provide compound 3 . The Z 1 group present in compound 3 may then be further transformed to provide the appropriate compounds of Formula III . In general, the alkylating agent 2 can be prepared using methods and techniques outlined in US Patent 5,177,095. More specifically, compound 2 (where Z 1 is COOR and Q is Br) can be synthesized from the substituted arylacetic acids 4 as outlined in Scheme 2 . The substituted arylacetic acid 4 is converted to the corresponding ester either by refluxing the acid in an appropriate alcohol in the presence of a catalytic amount of conc. sulfuric acid, or using other conventional methods of esterification. The resulting ester is then refluxed in carbon tetrachloride with N-bromosuccinimide and a catalytic amount of a radical initiator (e.g., AIBN or benzoylperoxide) to provide the 2-bromo-arylacetic acid ester 5 . Alternatively, the ester 5 may also be prepared from appropriate aryl aldehydes ( Scheme 3 ). The aldehyde 6 can be reacted with trimethylsilyl cyanide and catalytic amounts of KCN and 18-crown-6 to provide the corresponding trimethlylsilyl cyanohydrin 7 , which upon further treatment with the gaseous HCl and alcohol affords the 2-hydroxy ester 8 . The ester 8 is treated with triphenylphosphine and carbon tetrabromide in methylene chloride to give the 2-bromoarylacetate derivatives 5 . Scheme 4 outlines a typical synthesis of α-bromoarylacetates, 30 and 32 ,bearing appropriately substituted methylenedioxy or 1,4-dioxane rings. The substituted catechol derivative 27 is treated with an appropriate dibromide (where m is 1 or 2) in the presence of cesium carbonate in dimethylformamide to provide 28 . Treatment of 28 with DIBALH yields the aldehyde 29 which is then transformed into the desired alkyl bromide as described. The reactions are performed in a solvent appropriate to the reagents and materials employed and suitable for the transformation being effected. It is understood by those skilled in the art of organic synthesis that the functionality present on the heterocycle and in the reactants being employed should be consistent with the chemical transformations being conducted. Depending upon the reactions and techniques employed, optimal yields may require changing the order of synthetic steps or use of protecting groups followed by deprotection. The compounds useful in the novel method treatment of this invention form salts with various inorganic and organic acids and bases which are also within the scope of the invention. Such salts include ammonium salts, alkali metal salts like sodium and potassium salts, alkaline earth metal salts like the calcium and magnesium salts, salts with organic bases; e.g., dicyclohexylamine salts, N-methyl-D-glucamine, salts with amino acids like arginine, lysine, and the like. Also, salts with organic and inorganic acids may be prepared; e.g., HCl, HBr, H 2 SO 4 , H 3 PO 4 , methanesulfonic, toluenesulfonic, maleic, fumaric, camphorsulfonic. The salts can be formed by conventional means, such as by reacting the free acid or free base forms of the product with one or more equivalents of the appropriate base or acid in a solvent or medium in which the salt is insoluble, or in a solvent such as water which is then removed in vacuo or by freeze-drying or by exchanging the cations of an existing salt for another cation on a suitable ion exchange resin. It will be appreciated that the compounds of general Formula III in this invention may be derivatised at functional groups to provide prodrug derivatives which are capable of conversion back to the parent compounds in vivo . The concept of prodrug administration has been extensively reviewed (e.g. A.A. Sinkula in Annual Reports in Medicinal Chemistry , Vol 10, R.V. Heinzelman, Ed., Academic Press, New York London, 1975, Ch. 31, pp. 306-326, H. Ferres, Drugs of Today , Vol 19, 499-538 (1983) and J. Med. Chem. , 18, 172 (1975)). Examples of such prodrugs include the physiologically acceptable and metabolically labile ester derivatives, such as lower alkyl (e.g. methyl or ethyl esters), aryl (e.g. 5-indanyl esters), altenyl (e.g. vinyl esters), alkoxyalkyl (e.g. methoxymethyl esters), alkylthioalkyl (e.g. methylthiomethyl esters), alkanoyloxyalkyl (e.g. pivaloyloxymethyl esters), and substituted or unsubstituted aminoethyl esters (e.g. 2-dimethylaminoethyl esters). Additionally, any physiologically acceptable equivalents of the compounds of general Formula III, similar to the metabolically labile esters, which are capable of producing the parent compounds of general Formula III in vivo , are within the scope of this invention. It will be further appreciated that the majority of compounds of general Formula III claimed herein are asymmetric and are produced as racemic mixtures of enantiomers and that both the racemic compounds and the resolved individual enantiomers are considered to be within the scope of this invention. The racemic compounds of this invention may be resolved to provide individual enantiomers utilizing methods known to those skilled in the art of organic synthesis. For example, diastereoisomeric salts, esters or imides may be obtained from a racemic compound of general Formula III and a suitable optically active amine, amino acid, alcohol or the like. The diastereoisomeric salts, esters or imides are separated and purified, the optically active enantiomers are regenerated and the preferred enantiomer is the more potent isomer. The resolved enantiomers of the compounds of general Formula III, their pharmaceutically acceptable salts and their prodrug forms are also included within the scope of this invention. Endothelin (ET-1), and two closely related bioactive peptides, ET-2 and ET-3, are widely distributed in mammalian tissues, and they can induce numerous biological responses in non-vascular as well as vascular tissues by binding to at least two distinct endothelin receptor subtypes. In addition to cardiovascular smooth muscle, neural and atrial sites, endothelin receptors may also be found in gastrointestinal, kidney, lung, urogenital, uteral and placental tissues. Endothelin is a potent vasoconstrictor peptide and thus plays a role in vivo in arterial pressure-volume homeostasis. Not only peripheral, but coronary vascular resistance as well, is increased by endothelin; cardiac output is decreased, while plasma renin activity is increased. There is a reduction in renal blood flow and glomerular filtration rate, while levels of atrial natriuretic factor, vasopressin, and aldosterone become elevated. It is also considered, in accordance with the present invention, that antagonists for the endothelin receptor may be useful in preventing or reducing restenosis subsequent to denudation following angioplasty. Such denudation results in myointimal thickening following angioplasty, due to increased endothelin release. Endothelin acts as a growth factor with respect to smooth muscle and fibroblastic cells, and possibly other types of cells, as well. Endothelin is also a neuropeptide, acting on the posterior pituitary, where it modulates the release of the neurosecretory hormones vasopressin and oxytocin. Endothelin released from the posterior pituitary also acts as a circulating hormone, having a wide range of actions as discussed further above. This includes effects on the endocrine system, especially the adrenal glands. Endothelin increases plasma levels of epinephrine. Consequently, the novel compounds of the present invention, which are receptor antagonists of endothelin, have therapeutic usefulness in preventing, decreasing or modulating the various physiological effects of endothelin discussed above, by wholly or partially blocking access of endothelin to its receptor. Endothelin Receptor Binding Assays The binding of the novel compounds of this invention to the endothelin receptor was determined in accordance with the assay described in detail immediately below. It is similar to the assay described in Ambar et al. (1989) Biochem. Biophys. Res. Commun. 158 , 195-201; and Khoog et al. (1989) FEBS Letters, 253 , 199-202. The endothelins (ETs) have a number of potent effects on a variety of cells, and exert their action by interacting with specific receptors present on cell membranes. The compounds described in the present invention act as antagonists of ET at the receptors. In order to identify ET antagonists and determine their efficacy in vitro , the following three ligand receptor assays were established. Receptor binding assay using cow aorta membrane preparation: Thoracic aortae were obtained from freshly slaughtered calves and brought to the lab on wet ice. The adventitia were removed, and the aorta was opened up lengthwise. The lumenal surface of the tissue was scrubbed with cheesecloth to remove the endothelial layer. The tissue was ground in a meat grinder, and suspended in ice-cold 0.25 M sucrose, 5 mM tris-HCl, pH 7.4, containing 0.5 mg/mL leupeptin and 7 mg/mL pepstatin A. Tissue was homogenized twice and then centrifuged for 10 minutes at 750 x g at 4°C. The supematant was filtered through cheesecloth and centrifuged again for 30 minutes at 48,000 x g at 4°C. The pellet thus obtained was resuspended in the buffer solution described above (including the protease inhibitors), and aliquots were quick-frozen and stored at -70°C until use. Membranes were diluted into 50 mM KPi, 5 mM EDTA pH 7.5 containing 0.01% human serum albumin. Assays were done in triplicate. Test compounds and 100 pM [ 125 I]-endothelin-1 (2000-2200 Ci/mmole, obtained from New England Nuclear or Amersham) were placed in a tube containing this buffer, and the membranes prepared above were added last. The samples were incubated for 60 min at 37°C. At the end of this incubation, samples were filtered onto prewetted (with 2% BSA in water) glass fiber filter pads and washed with 150 mM NaCl, 0.1% BSA. The filters were assayed for 125 I radioactivity in a gamma counter. Nondisplaceable binding of [ 125 I]-endothelin-1 is measured in the presence of 100 nM unlabelled endothelin-1 [Endothelin-1 (ET-1) was purchased from Peptides International (Louisville, KY). 125 I-ET-1 (2000 Ci/mMol) was purchased from Amersham (Arlington Heights, IL)]. Specific binding is total binding minus nondisplaceable binding. The inhibitory concentration (IC 50 ) which gives 50% displacement of the total specifically bound [ 125 I]-endothelin-1 was presented as a measure of the efficacy of such compounds as ET antagonists. Receptor binding assay using rat hippocampal membrane preparation: Rat hippocampi were obtained from freshly sacrificed male Sprague-Dawley rats and placed in ice cold 0.25 M sucrose, 5 mM tris-HCl, pH 7.4 containing 0.5 mg/mL leupeptin, 7 mg/mL pepstatin A. Hippocampi were weighed and placed in a Dounce homogenizer with 25 volumes (wet weight to volume) ice-cold sucrose buffer in the presence of protease inhibitors. Hippocampi were homogenized using a Dounce (glass-glass) homogenizer with type A pestle, with homogenizer in ice. Tissue homogenate was centrifuged at 750 x g for 10 min at 4°C. Supernatant was filtered through dampened cheesecloth, and centrifuged again at 48,000 x g for 30 mm at 4°C. Pellets were resuspended in sucrose buffer with protease inhibitors. Aliquots of this preparation were quick frozen and stored at -70°C until use. Membranes were diluted into 50 mM KPi, 5 mM EDTA pH 7.5 containing 0.01% human serum albumin. Assays were done in triplicate. Test compounds and 25 pM [ 125 I]-endothelin-1 (2000-2200 Ci/mmole, obtained from New England Nuclear or Amersham) were placed in a tube containing this buffer, and the membranes prepared above were added last. The samples were incubated for 60 min at 37°C. At the end of this incubation, samples were filtered onto prewetted (with 2% BSA in water) glass fiber filter pads and washed with 150 mM NaCl, 0.1% BSA. The filters were assayed for 125 I radioactivity in a gamma counter. Nondisplaceable binding of [ 125 I]-endothelin-1 is measured in the presence of 100 nM unlabelled endothelin-1 [Endothelin-1 (ET-1) was purchased from Peptides Intemational (Louisville, KY). 125 I-ET-1 (2000 Ci/mMol) was purchased from Amersham (Arlington Heights, IL)]. Specific binding is total binding minus nondisplaceable binding. The inhibitory concentration (IC 50 ) which gives 50% displacement of the total specifically bound [ 125 I]-endothelin-1 was presented as a measure of the efficacy of such compounds as endothelin antagonists. Receptor binding assay using cloned human ET receptors expressed in Chinese Hamster Ovary Cells: Both endothelin receptor subtypes were cloned from a human cDNA library and were individually expressed in Chinese Hamster Ovary cells. Cells were harvested by addition of 126 mM NaCl, 5 mM KCl, 2 mM EDTA, 1 mM NaH 2 PO 4 , 15 mM glucose, 10 mM tris/HEPES pH 7.4 Cells were centrifuged at 250 x g for 5 minutes. The supernatant was aspirated off, and the cells were resuspended in the 50 mM KPi, 5 mM EDTA pH 7.5 containing 0.01% human serum albumin. Assays were done in triplicate. Test compounds and 25-100 pM [ 125 I]-endothelin-1 (2000-2200 Ci/mmole, obtained from New England Nuclear or Amersham) were placed in a tube containing 50 mM KPi, 5 mM EDTA pH 7.5 containing 0.01% human serum albumin, and the cells prepared above were added last. The samples were incubated for 60 mm at 37°C. At the end of this incubation, samples were filtered onto prewetted (with 2% BSA in water) glass fiber filter pads and washed with 150 mM NaCl, 0.1% BSA. The filters were assayed for 125 I radioactivity in a gamma counter. Nondisplaceable binding of [ 125 I]-endothelin-1 is measured in the presence of 100 nM unlabelled endothelin-1 [Endothelin-1 (ET-1) was purchased from Peptides International (Louisville, KY). 125 I-ET-1 (2000 Ci/mMol) was purchased from Amersham (Arlington Heights, IL)]. Specific binding is total binding minus nondisplaceable binding. The inhibitory concentration (IC 50 ) which gives 50% displacement of the total specifically bound [ 125 I]-endothelin-1 was presented as a measure of the efficacy of such compounds as endothelin antagonists. The binding assays described above were used to evaluate the potency of interaction of representative compounds of the invention with endothelin receptors. To determine whether these compounds were endothelin antagonists, assays which measure the ability of the compounds to inhibit endothelin-stimulated phosphatidylinositol hydrolysis were established. Rat uterus contains predominantly one of the known endothelin receptor subtypes (ET A ). Phosphatidylinositol hydrolysis assays using rat uterine slices: Diethylstilbestrol primed female Sprague-Dawley rats were sacrificed and their uteri were collected, dissected of fat and connective tissue and minced. Minced tissue was added to oxygenated (95% O 2 , 5% CO 2 ) 127 mM NaCl, 25 mM NaHCO 3 , 10 mM Glucose, 2.5 mM KCl, 1.2 mM KH 2 PO 4 , 1.2 mM MgSO 4 , 1.8 mM CaCl 2 . To the tissue mince, 1.2 mM myo-[ 3 H]-inositol (Amersham) was added. The mince was incubated 90 min at 37°C, with constant oxygenation. After incubation, the loaded tissue mince was washed five times with the same oxygenated buffer to remove excess radiolabelled inositol. The tissue mince was resuspended in the above buffer, containing 10 mM LiCl, aliquotted into tubes, and 3 nM endothelin-1 with and without test compounds was added to start the assay. Assays were done in quadruplicate. Samples were incubated at 37°C under blowing O 2 in a hooded water bath for 30 minutes. Reaction was stopped by addition of trichioroacetic acid to 6% concentration. Samples were sonicated for 10 min, centrifuged 20 min, then trichloroacetic acid was extracted with water-saturated ethyl ether. An aliquot of each sample was neutralized and diluted by addition of 50 mM tris-HCl pH 7.4. A 100 mL aliquot of this solution was assayed for radioactivity in a beta counter. The diluted neutralized sample was applied to Dowex 1 x 8-formate columns, washed with water, then washed with 60 mM ammonium formate, 5 mM sodium tetraborate. Samples were eluted with 200 mM ammonium formate, 5 mM sodium tetraborate. The radioactivity of each eluted sample was measured in a beta counter. Radioactivity was normalized by dividing radioactivity in post column sample by radioactivity in precolumn sample. Control values (100% stimulated) are values in the presence of endothelin minus the values in the absence of endotelin (basal). Test sample values are the values in the presence of endothelin and test sample minus basal. Inhibitory concentration (IC 50 ) is the concentration of test compound required to give a sample activity of 50% of control value. Sarafotoxin S6c is a member of the endothelin family which binds preferentially to one of the known endothelin receptor subtypes (ET B ). Phosphatidylinositol hydrolysis assays using rat lung slices: Male Sprague-Dawley rats were sacrificed and their lungs were collected, dissected of fat and connective tissue and minced. Minced tissue was added to oxygenated (95% O 2 , 5% CO 2 ) 127 mM NaCl, 25 mM NaHCO 3 , 10 mM glucose, 2.5 mM KCl, 1.2 mM KH 2 PO 4 , 1.2 mM MgSO 4 , 1.8 mM CaCl 2 . To the tissue mince, 1.2 µM myo -[ 3 H]-inositol was added. The mince was incubated 60 min at 37°C, with constant oxygenation. After incubation, loaded tissue mince was washed five times with the same oxygenated buffer to remove excess radiolabelled inositol. Tissue mince was resuspended in the above buffer, containing 10 mM LiCl, aliquotted into tubes, and 3 nM sarafotoxin S6c with and without test compounds was added to start the assay. Assays were done in quadruplicate. Samples were incubated at 37°C under blowing O 2 in a hooded water bath for 30 minutes. Reaction was stopped by addition of 0.5 mL 18% trichloroacetic acid to 6% concentration. Samples were sonicated for 10 min, centrifuged 20 min, then trichloroacetic acid was extracted with water-saturated ethyl ether. An aliquot of each sample was neutralized and diluted by addition of 50 mM tris-HCl pH 7.4. A 100 mL aliquot of this solution was assayed for radioactivity in a beta counter. The diluted neutralized sample was applied to Dowex 1 x 8-formate columns, washed with water, then washed with 60 mM ammonium formate, 5 mM sodium tetraborate. Samples were eluted with 200 mM ammonium formate, 5 mM sodium tetraborate. The radioactivity of each eluted sample was measured in a beta counter. Radioactivity was normalized by dividing radioactivity in post column sample by radioactivity in precolumn sample. Control values (100% stimulated) are values in the presence of sarafotoxin minus the values in the absence of sarafotoxin (basal). Test sample values are the values in the presence of sarafotoxin and test sample minus basal. Inhibitory concentration (IC 50 ) is the concentration of test compound required to give a sample activity of 50% of control value. Phosphatidylinositol hydrolysis assays using cloned human endothelin receptors expressed in Chinese Hamster Ovary cells: Endothelin receptors of both receptor subtypes were cloned from a human cDNA library and were individually expressed in Chinese Hamster Ovary cells. Cells were loaded overnight by the addition of 1.2 µM myo -[ 3 H]-inositol to their growth medium. Cells were harvested by addition of 126 mM NaCl, 5 mM KCl, 2 mM EDTA, 1 mM NaH 2 PO 4 , 15 mM glucose, 10 mM tris/HEPES pH 7.4. Cells were washed five times by centrifugation at 250 x g for 5 minutes to remove excess radiolabelled inositol. The supematant was aspirated off, and the cells were resuspended in the same oxygenated (95% O 2 , 5% CO 2 ) buffer containing 10 mM LiCl, aliquotted into tubes, and 0.3 nM endothelin-1 with and without test compounds was added to start the assay. Assays were done in quadruplicate. Samples were incubated at 37°C under blowing O 2 in a hooded water bath for 30 minutes. Reaction was stopped by addition of 0.5 mL 18% trichioroacetic acid to 6% concentration. Samples were sonicated for 10 mm, centrifuged 20 min, then trichioroacetic acid was extracted with water-saturated ethyl ether. An aliquot of each sample was neutralized and diluted by addition of 50 mM tris-HCl pH 7.4. A 100 mL aliquot of this solution was assayed for radioactivity in a beta counter. The diluted neutralized sample was applied to Dowex 1 x 8-formate columns, washed with water, then washed with 60 mM ammonium formate, 5 mM sodium tetraborate. Samples were eluted with 200 mM ammonium formate, 5 mM sodium tetraborate. The radioactivity of each eluted sample was measured in a beta counter. Radioactivity was normalized by dividing radioactivity in post column sample by radioactivity in precolumn sample. Control values (100% stimulated) are values in the presence of endothelin minus the values in the absence of endothelin (basal). Test sample values are the values in the presence of endothelin and test sample minus basal. Inhibitory concentration (IC 50 ) is the concentration of test compound required to give a sample activity of 50% of control value. Using the methodology described above, representative compounds of the invention were evaluated and found to exhibit IC 50 values of at least <50 µM thereby demonstrating and confirming the utility of the compounds of the invention as effective endothelin antagonists. Intravenous Effect of Endothelin-1 Antagonist, N -(4- iso -propylbenzenesulfonyl)-α-(4-carboxy-2- n -propylphenoxy)-3,4-methylenedioxyphenylacetamide dipotassium salt [Example 42] on Endothelin 1-Induced Changes, in Diastolic and Urethral Pressures in the Anesthetized Male Dog Methodology for determining whether an ET-1 selective antagonist could inhibit the ET-1 mediated prostatic urethral contractions in a mongrel dog model: On separate days, two fasted male mongrel dogs (HRP, Inc.) weighing 11.0 and 12.4 kg, were anesthetized with Sodium Pentobarbital (Steris Laboratories, Inc.) at 35 mg/kg (i.v.) to effect, followed by 4 mg/kg/hr (i.v.) infusion. A cuffed endotracheal tube was inserted and each animal was ventilated with room air using a positive displacement large animal ventilator (Harvard Apparatus) at a rate of 18 breaths/minute and an average tidal volume of 18 ml/kg body weight. Body temperature was maintained with a heating pad and heat lamp using a temperature controller (YSI) and esophageal probe. Two catheters (PE 260) were placed in the aorta via the femoral arteries (one in each artery) for administration of endothelin or phenylephrine and for continuous direct monitoring of blood pressure and heart rate using a Statham blood pressure transducer (Spectramed) and a computer system (Modular Instruments, Inc.). Two other catheters (PE 260) were placed in the vena cava via the femoral veins (one catheter in each vein) for administration of pentobarbital and N -(4- iso -propylbenzenesulfonyl)-α-(4-carboxy-2- n -propylphenoxy)-3,4-methylenedioxyphenylacetamide dipotassium salt [Example 42]. A supra-pubic incision approximately one-half inch lateral to the penis was made to expose the ureters, urinary bladder, prostate, and urethra. The dome of the bladder was retracted to facilitate dissection of the ureters. The ureters were cannulated with PE 90 and tied off to the bladder. Umbilical tape was passed beneath the urethra at the bladder neck and another piece of tape was placed approximately 1-2 cm. distal to the prostate. The bladder dome was incised and a Micro-tip® catheter transducer (Millar Instruments, Inc.) was advanced into the urethra. The neck of the bladder was ligated with the umbilical tape to hold the transducer. The bladder incision was sutured wit 3-0 silk (purse string suture). The transducer was withdrawn until it was positioned in the prostatic urethra. The position of the Micro-tip® catheter was verified by gently squeezing the prostate and noting the large change in urethral pressure prior to ligating the distal urethra. Experimental Protocol: Phenylephrine (PB) (10 µg/kg, intra-arterial) was administered and pressor effects on diastolic blood pressure (DBP) and intra-urethral pressure (IUP) were noted. When blood pressure returned to baseline, endothelin-1 (ET-1) (1 nmole/kg, intra-arterial) was administered. Changes in DBP and IUP were monitored for one hour and an ET-1 selective endothelin antagonist, such as the compound of Example 42, N -(4- iso -propylbenzene-sulfonyl)-α-(4-carboxy-2- n -propylphenoxy)-3,4-methylenedioxyphenyl-acetamide dipotassium salt (30 mg/kg, intra-venous) was administered. Ten to fifteen minutes later when blood pressure had stabilized, ET-1 was administered again, and inhibition of ET-1 induced effects were noted. PE was administered at the end of the experiment to verify specificity for ET-1 blockade. The dogs were euthanized with an overdose of pentobarbital followed by saturated KCl. The drugs utilized in the experiment described above were: 1) Phenylephrine, HCl (PE) (Sigma Chemical, Co.) was given at a volume of 0.05 mL/kg; 2) Endothelin-1 (ET-1) (Human, Porcine, Canine, Rat, Mouse, Bovine) (Peninsula Laboratories, Inc.) was given at a volume of 0.05 mL/kg; 3) ET-1 selective antagonist, such as the compound of Example 58, N -(4- iso -propylbenzene-sulfonyl)-α-(4-carboxy-2- n -propylphenoxy)-3,4-methylenedioxyphenylacetamide dipotassium salt, was given at a volume of 0.3 mL/kg. All drugs were dissolved in isotonic saline solution. Results: ET-1 elicited an initial depressor effect followed by a longer pressor effect. In one dog, the pressor effect was biphasic. The decrease in DBP in both dogs averaged 13 mmHg, while the peak pressor effect averaged 26 mmHg. The average ET-1 induced increase in IUP was 15 mmHg. Ten to 14 minutes after administration of N -(4- iso- propylbenzene-sulfonyl)-α-(4-carboxy-2- n -propylphenoxy)-3,4-methylenedioxyphenyl-acetamide dipotassium salt [Example 58], the dogs were challenged with ET-1 again and the depressor and pressor effects on DBP were inhibited 69% and 76%, respectively. The pressor effect on IUP was inhibited 93% (Table 1). Intra-arterial PE-induced increases in DBP and IUP did not change significantly after administration of N -(4- iso -propylbenzene-sulfonyl)-α-(4-carboxy-2- n -propylphenoxy)-3,4-methylenedioxyphenyl-acetamide dipotassium salt [Example 42] in the one dog studied. Increases in DBP and IUP were inhibited 35 and 13%, respectively (Table 2). Effects of ET-1 Antagonist, N -(4- iso -propylbenzenesulfonyl)-α-(4-carboxy-2- n -propylphenoxy)-3,4-methylenedioxyphenylacetamide dipotassium salt [Example 42], on ET-1 Induced Changes in DBP and IUP in Anesthetized Male Dogs (n=2) CHANGE IN DBP (mmHg) CHANGE IN IUP (mmHg) DOG # DEPRESSOR PRESSOR PRESSOR ET-1 (i.a.) HG FMJC -10 19 18 HG FMHK -15 33 11 MEAN -13 26 15 SEM 3 7 4 ET-1 + Example 42 HG FMJC -3 8 1 HG FMHK -5 2 1 MEAN -4 5 1 SEM 1 3 0 % INHIBITION HG FMJC 70 58 94 HG FMHK 67 94 91 MEAN 69 76 93 SEM 2 18 2 Effects of ET-1 Antagonist, N -(4- iso -propylbenzenesulfonyl)-α-(4-carboxy-2- n -propylphenoxy)-3,4-methylenedioxyphenylacetamide dipotassium salt [Example 42], on PE-Induced Changes in DBP and IUP in Anesthetized Male Dog # HG FMJC TREATMENT INCREASE IN DBP (mmHg) INCREASE IN IUP (mmHg) Phenylephrine 17 31 Phenylephrine + Example 58 11 27 % Inhibition of Control 35 13 Conclusions : ET-1 causes constriction of the prostatic urethra, as well as a complex hemodynamic response comprised of an initial depressor and subsequent pressor response in anesthetized dogs. The hemodynamic and prostafic urethral responses to ET-1 were specifically inhibited by N -(4- iso -propylbenzenesulfonyl)-α-(4-carboxy-2- n -propylphenoxy)-3,4-methylenedioxyphenylacetamide dipotassium salt. The efficacy of the N -(4- iso -propylbenzenesulfonyl)-α-(4-carboxy-2- n -propylphenoxy)-3,4-methylenedioxyphenylacetamide dipotassium salt in inhibiting the prostatic urethral pressor effect of ET-1 suggests that selective antagonists of ET-1 will be useful in the treatment of urinary obstruction in benign prostatic hyperplasia. In Situ Rat Prostate : Male Sprague-Dawley rats (Taconic Farms) weighing 300-400 grams were anesthetized with urethane (1.75 g/kg, ip), a tracheal cannula was inserted, and the femoral artery was cannulated. Core body temperature was maintained at 37 + 0.5 °C. A 4-5 cm midline abdominal incision was made to expose the bladder and prostate. The prostate was separated from the bladder and surrounding capsule by blunt dissection with a forcep. A length of surgical silk was gently secured around the anterior tips of the prostate lobes. A second length of surgical silk attached to an atraumatic needle was passed through and tied to the base of the prostate approximately 10-12 mm posterior to the first tie. The posterior ligature was secured to an anchor post whereas the anterior ligature was connected to a Grass FT03 transducer (Grass Instruments, Quincy, MA) and maintained at a tension of 1 g. Signals from the transducer were amplified and recorded on a polygraph (Hewlett-Packard 8805B amplifiers and 7758A recorder, Palo Alto, CA). After equilibrating for approximately 15 min, the rats were administered pretreatment drugs (atropine 1 mg/kg, (+) propranolol 1 mg/kg) 10 min apart through the intra-arterial (IA) cannula. Thirty minutes later, ET-1 (0.3 nmoles/kg) was injected intra-arterial every thirty minutes for a total of three times. Five minutes before the third injection of ET-1, vehicle with or without an endothelin antagonist was injected IA. The response of the prostate to FT-1 was quantified by measuring the change (Δ) from baseline tension to the peak of the response during the 5-minute period after the third FT-1 injection. The in situ rat postate protocol has been utilized to determine the antagonist activity and potency of compounds of this invention to block the direct contractile effects of FT-1 on the rat prostate in vivo. In this protocol, N -(4- iso -propylbenzene-sulfonyl)-α-(4-carboxy-2- n -propylphenoxy)-3,4-methylenedioxyphenylacetamide dipotassium salt was demonstrated to cause a specific inhibition of FT-1 to contract the prostate and will be useful in the treatment of urinary obstruction in benign prostatic hyperplasia. Accordingly the novel compounds of the present invention are useful in human therapy for treating asthma, hypertension, renal failure particularly post-ischemic renal failure, cyclosporin nephrotoxicity, vasospasm, cerebral and cardiac ischemia, myocardial infarction, or endotoxin shock caused by or associated with endothelin, by adminstration to a patient in need of such treatment of a therapeutically effective amount thereof. In the management of hypertension and the clinical conditions noted above, the compounds of this invention may be utilized in compositions such as tablets, capsules or elixirs for oral administration, suppositories for rectal administration, sterile solutions or suspensions for parenteral or intramuscular administration, and the like. The compounds of this invention can be administered to patients (animals and human) in need of such treatment in dosages that will provide optimal pharmaceutical efficacy. Although the dose will vary from patient to patient depending upon the nature and severity of disease, the patient's weight, special diets then being followed by a patient, concurrent medication, and other factors which those skilled in the art will recognize, the dosage range will generally be about 0.5 mg to 1.0 g. per patient per day which can be administered in single or multiple doses. Perferably, the dosage range will be about 0.5 mg to 500 mg. per patient per day; more preferably about 0.5 mg to 200 mg. per patient per day. The compounds of this invention can also be administered in combination with A2-adrenosine receptor agonists, α-adrenergic antagonists, angiotensin II antagonists, angiotensin converting enzyme inhibitors, β-adrenergic antagonists, atriopeptidase inhibitors(alone or with ANP), calcium channel blockers, diuretics, potassium channel agonists, renin inhibitors, sertonin antagonists, sympatholytic agents, as well as other antihypertensive agents. For example, the compounds of this invention can be given in combination with such compounds as A-69729, FK 906, FK 744, UK-73900, CSG 22492C, amiloride, atenolol, atriopeptin, bendroflumethiazide, chlorothalidone, chlorothiazide, clonidine, cromakalin, cryptenamine acetates and cryptenamine tannates, deserpidine, diazoxide, doxazosin, guanabenz, guanethidine, guanethidine sulfate, hydralazine hydrochloride, hydrochlorothiazide, isradipine, ketanserin, losartan, metolazone, metoprolol, metoprolol tartate, methyclothiazide, methyldopa, methyldopate hydrochloride, minoxidil, nadolol, pargyline hydrochloride, pinacidil, pindolol, polythiazide, prazosin, propranolol, rauwolfia serpentina , rescinnamine, reserpine, sodium nitroprusside, spironolactone, terazosin, timolol maleate, trichlormethiazide, trimethophan camsylate, verapamil, benzthiazide, quinethazone, ticrynafan, triamterene, acetazolamide, aminophylline, cyclothiazide, ethacrynic acid, furosemide, merethoxylline procaine, sodium ethacrynate, captopril, delapril hydrochloride, enalapril, enalaprilat, fosinopril sodium, lisinopril, pentopril, quinapril, quinapril hydrochloride, ramapril, teprotide, zofenopril, zofenopril calcium, diflusinal, diltiazem, felodipine, nicardipine, nifedipine, niludipine, nimodipine, nisoldipine, nitrendipine, and the like, as well as admixtures and combinations thereof. Combinations useful in the management of congestive heart failure include, in addition, compounds of this invention with cardiac stimulants such as dobutamine and xamoterol and phosphodiesterase inhibitors including antnone and milrinone. Typically, the individual daily dosages for these combinations can range from about one-fifth of the minimum recommended clinical dosages to the maximum recommended levels for those entities given singly. To illustrate these combinations, one of the endothelin antagonists of this invention effective clinically at a given daily dose range can be effectively combined, at levels which are less than that daily dose range, with the following compounds at the indicated per day dose range: hydrochlorothiazide (6-100 mg), chlorothiazide (125-500 mg), furosemide(5-80 mg), ethacrynic acid (5-200 mg), amiloride (5-20 mg), diltiazem(30-540 mg), felodipine(1-20 mg), nifedipine(5-120 mg), nitrendipine(5-60 mg), timolol maleate (1-20 mg), propanolol (10-480 mg), and methyldopa(125-2000 mg). In addition triple drug combinations of hydrochlorothiazide(6-100 mg) plus amiloride (5-20 mg) plus endothelin antagonists of this invention, or hydrochlorothiazide(6-100 mg) plus timolol maleate (1-20 mg) plus endothelin antagonists of this invention, or hydrochlorothiazide(6-100 mg) plus nifedipine (5-60 mg) plus endothelin antagonists of this invention are effective combinations to control blood pressure in hypertensive patients. Naturally, these dose ranges can be adjusted on a unit basis as necessary to permit divided daily dosage and the dose will vary depending on the nature and severity of the disease, weight of the patient, special diets and other factors. The present invention also relates to pharmaceutical compositions for treating asthma, hypertension, renal failure, particularly post-ischemic renal failure, cyclosporin nephrotoxicity, vasospasm, cerebral and cardiac ischemia, benign prostatic hyperplasia, myocardial infarction, or endotoxin shock caused by or associated with endothelin, comprising a therapeutically effective amount of the novel compound of this invention together with a pharmaceutically acceptable carrier therefor. About 0.5 mg to 1.0 g. of compound or mixture of compounds of Formula III or a physiologically acceptable salt is compounded with a physiologically acceptable vehicle, carrier, excipient, binder, preservative, stabilizer, flavor, etc., in a unit dosage form as called for by accepted pharmaceutical practice. The amount of active substance in these compositions or preparations is such that a suitable dosage in the range indicated is obtained. Illustrative of the adjuvants which can be incorporated in tablets, capsules and the like are the following: a binder such as gum tragacanth, acacia, corn starch or gelatin; an excipient such as microcrystalline cellulose; a disintegrating agent such as corn starch, pregelatinized starch, alginic acid and the like; a lubricant such as magnesium stearate; a sweetening agent such as sucrose, lactose or saccharin; a flavoring agent such as peppermint, oil of wintergreen or cherry. When the dosage unitform is a capsule, it may contain, in addition to materials of the above type, a liquid carrier such as fatty oil. Various other materials may be present as coatings or to otherwise modify the physical form of the dosage unit. For instance, tablets may be coated with shellac, sugar or both. A syrup or elixir may contain the active compound, sucrose as a sweetening agent, methyl and propyl parabens as preservatives, a dye and a flavoring such as cherry or orange flavor. Sterile compositions for injection can be formulated according to conventional pharmaceutical practice by dissolving or suspending the active substance in a vehicle such as water for injection, a naturally occurring vegetable oil like sesame oil, coconut oil, peanut oil, cottonseed oil, etc., or a synthetic fatty vehicle like ethyl oleate or the like. Buffers, preservatives, antioxidants and the like can be incorporated as required. The following examples illustrate the preparation of the compounds of Formula III and their incorporation into pharmaceutical compositions and as such are not to be considered as limiting the invention set forth in the claims appended hereto. EXAMPLE 1 (Reference) 2-(2,6-Dipropyl-4-hydroxymethyl)phenoxyphenylacetic acids Step A : Preparation of Alkyl 2-bromo-2-phenylacetates Method A : Substituted phenylacetic acid is convered to the corresponding methyl ester by refluxing the acid in methanol in the presence of a catalytic amount of conc. sulfuric acid. The ester thus obtained is then refluxed in carbon tetrachioride with N-bromosuccinimide (1.1 equiv) and AIBN (0.05-0.1 equiv). Upon completion of the reaction, the resulting product is purified by flash column chromatography using silica gel and ethyl acetate in hexane as eluent to provide the desired alkyl bromide. Method B : An arylaldehyde is reacted overnight with trimethylsilyl cyanide in the presence of catalytic amounts of KCN and 18-crown-6 in methylene chloride. The reaction mixture is quenched with water and extracted with CH 2 Cl 2 / ethyl acetate/ether (1/2/2) mixture. The organic phase is washed with saturated aq. NaHCO 3 solution. After drying and concentration of the organic phase, the resulting trimethylsilyl cyanohydrin is hydrolyzed to give the corresponding hydroxy acid. Treatment with gaseous HCl in methanol or ethanol at 0°C for 0.5 h and then overnight at room temperature affords the crude 2-hydroxy ester. The ester is then treated with triphenylphosphine and carbon tetrabromide in methylene chloride at 0°C overnight. Methylene chloride is removed and flash column chromatography of the crude product using silica gel and ethyl acetate/hexane as eluent gives the desired 2-bromophenylacetates. Step B : Alkylation of the phenol (2,6-Dipropyl-4-hydroxymethyl)phenol (prepared as described in patent application WO 91/11999) is alkylated with 2-bromo-2-aryl esters in DMF using either cesium carbonate (Cs 2 CO 3 ), or potassium carbonate (K 2 CO 3 ), or sodium hydride (NaH). The alkylated product is purified by flash column chromatography using silica gel and ethyl acetate/hexane mixture as eluent to provide the desired substituted 2-phenoxy-2-phenylacetic acid esters. Step C : General procedure for ester hydrolysis The product of Step C is dissolved in methanol or ethanol and reacted with aqueous NaOH or LiOH, or KOH solution at room temperature for 1- 6 hours, neutralized to pH 7 with 1 N HCl and then concentrated in vacuo. The residue is purified on a silica gel flash chromatography column to afford the corresponding carboxylic acid. The following phenoxyphenylacetic acid derivatives were prepared using the general procedures outlined in Example 1 . EXAMPLE 2 2-[(2,6-Dipropyl-4-hydroxymethyl)phenoxyl-2-(3,4-ethylenedioxyphenyl)acetic acid 1 H NMR (200 MHz, CD 3 OD, ppm): δ 6.95 (m, 3H), 6.85 (dd, 1H, J=8.3, 2.0 Hz), 6.72 (d, 1H, J=8.3 Hz), 4.76 (s, 1H), 4.46 (s, 2H), 4.20 (s, 4H), 2.37 (t, 4H, J=7.9 Hz), 1.44 (m, 4H), 0.83 (t, 6H, J=7.3 Hz). FAB-MS m/e = 401 (M+1) EXAMPLE 3 2-[2,6-Dipropyl-4-hydroxymethyl)phenoxy]-2-(3,4-methylenedioxyphenyl)acetic acid 1 H NMR (200 MHz, CD 3 OD, ppm): δ 7.03 (s, 1H), 6.97 (s, 2H), 6.83 (d, 1H, J=7.7 Hz), 6.73 (d, 2H, J= 7.7 Hz), 5.94 (s, 2H), 4.84 (s, 1H), 4.48 (s, 2H), 2.38 (t, 4H, J=8.0 Hz), 1.46 (m, 4H), 0.85 (t, 6H, J=7.4 Hz). FAB-MS m/e = 387 (M+1) EXAMPLE 4 2-[(2,6-Dipropyl-4-hydroxymethyl)phenoxy]-2-(2-naphthyl)acetic acid 1 H NMR (400 MHz, CD 3 OD, ppm): δ 8.56-8.52 (m, 1H), 7.86-7.79 (m, 2H), 7.47-7.43 (m, 2H), 7.35-7.32 (m, 1 H), 6.91 (s, 2H), 5.36 (s, 1H), 4.44 (s, 1H), 1.46-1.41 (m, 2 H), 1.2-1.16 (m, 2H), 0.58 (t, J = 7.37, 6 H). EXAMPLE 5 2-[(2,6-Dipropyl-4-(2-hydroxyethyl)phenoxy]-2-(2-naphthyl)acetic acid STEP A : t-Butyldimethylsilyloxy-2,6-Dipropyl-4-formylbenzene To a solution of 5.03 g (15.4 mmol)of t-butyldimethylsilyloxy-2,6-dipropyl-4-hydroxymethyl benzene in 30 mL of methylene chloride was added 8.7 g of pyridinium dichromate (PDC). The reaction mixture was stirred for 3 hours and then diluted with 300 mL of ethyl ether. The solution was then filtered through a pad of a 1:1 mixture of florisil and celite. Concentration of the filtrate gave 4.85 g of the title compound. 1 H NMR (400 MHz, CDCl 3 , ppm): δ 9.8 (s, 1H), 7.51 (s, 2H), 2.59-2.55 (m, 2H) 1.59-1.55 (m, 2H), 0.99 (s, 9H), 0.91 (t, J = 7.28 Hz, 3H), 0.20 (s, 6H). STEP B : t-Butyldimethylsilyloxy-2,6-dipropyl-4-vinyl benzene To a solution of 1.0 g (2.80 mmol) of methyl triphenylphosphonium bromide in 5.0 mL of ether at 0°C was added 1.12 mL (2.5M, 2.80 mmol) of butyllithiuin. The reaction mixture was stirred for 30 minutes at 0°C and then 756 mg (2.33 mmol) of the title compound from Example 5 (Step A) was added. After stirring for 1h at room temperature, the reaction mixture was poured into ethyl acetate and washed with water and then saturated aqueous sodium chloride. The organic layer was dried over anhydrous sodium sulfate, filtered and concentrated. Purification by flash chromotography (silica gel, hexane / ethyl acetate 97:3) gave 411 mg of the title compound. 1 H NMR (400 MHz, CDCl 3 , ppm): δ 7.02 (s, 2H), 6.6 (dd, J = 17.6, J = 10.7 Hz, 1H), 5.55 (d, J=17.6 Hz, 1H), 5.08 (d, J = 10.7 Hz, 1H), 2.53-2.50 (m, 4 H), 1.59-1.53 (m, 4H), 0.996 (s, 9 H), 0.90 (t, J = 7.33 Hz, 6 H), 0.16 (s, 6 H). STEP C : t-Butyldimethylsilyloxy-2,6-dipropyl-4-(2-hydroxyethyl)benzene To a solution of 475 mg (1.48 inmol) of the product of Step B in 3 mL of THF at 0 °C was added 1.6 mL (1.62 mmol) of a 1N borane / THF solution. After 1 hour TLC indicated that the starting material had been consumed. The reaction mixture was quenched with 3 drops of methanol and then 0.70 mL (6.22 mmol) of 30 % sodium peroxide and 6.2 mL (6.2 mmol) of 1 N sodium hydroxide were added. After two hours the reaction mixture was diluted with ethyl acetate and washed with water and brine. The organic layer was then dried over sodium sulfate, filtered and concentrated. Flash chromatography (silica gel, hexane / ethyl acetate 4:1) gave 265 mg of the title compound as a clear oil. 1 H NMR (400 MHz, CDCl 3 , ppm): δ 6.79 (s, 2 H), 3.79 (m, 2 H), 2.75 - 2.72 (m, 2 H), 2.51 - 2.48 (m, 4 H), 1.58 - 1.51 (m, 6 H), 0.99 (s, 9 H), 0.90 (t, J = 7.33, 6 H), 0.16 (s, 6 H). STEP D : 2,6-Dipropyl-4-(2-hydroxyethyl)phenol To a solution of 1.0 g (2.98 mmol) of the product of Step C in 3.0 mL of THF was added 3.57 mL (3.57 mmol) of 1.0 N solution of tetrabutylammonium fluoride in THF. After 15 minutes TLC indicated that the reaction was complete. The reaction mixture was concentrated and then purified by flash chromatography (silica gel, hexane/ethyl acetate 3:1) to give 1.13 g of the title compound. 1 H NMR (400 MHz, CDCl 3 , ppm): δ 6.8 (s, 2 H) , 3.78 (t , J = 6.5 Hz, 2 H), 2.73 (t, J = 6.5 Hz, 2 H), 2.54 - 2.50 (m, 4H), 1.66 - 1.56 (m, 4 H), 0.96 (t , J = 7.3 Hz, 6 H). STEP E : Methyl 2-[(2,6-dipropyl-4-(2-hydroxyethyl)phenoxy]-2-(2-naphthyl)acetate The title compound was prepared from 2,6-dipropyl-4-(2-hydroxyethyl)phenol (Step D) by alkylating with methyl 2-bromo-2-(2-naphthyl)acetate using cesium carbonate or potassium carbonate in DMF. The reaction mixture was filtered through Celite and the filter cake was washed with methylene chloride. The filtrate was concentrated and the resultant material was purified by flash column chromatography to yield the titled ester. 1 H NMR (400 MHz, CDCl 3 , ppm): δ 7.90 - 7.82 (m, 4 H) , 7.69 - 7.67 (m, 1 H) , 7.49 - 7.47 (m, 2H) , 6.8 (s, 2 H), 2.74 (t, J = 6.2 Hz, 2 H), 2.36-2.32 (m, 4 H), 1.49 - 1.41 (m, 4 H), 0.72 (t, J = 7.3, 6 H). STEP F : 2-[(2,6-Dipropyl-4-(2-hydroxyethyl)phenoxy]-2-(2-naphthyl)acetic acid The title compound was prepared from the product of Step E by saponification with 1N aqueous KOH in methanol as outlined in Step C of Example 1. 1 H NMR (400 MHz, CD 3 OD, ppm) δ 7.84 - 7.7 (m, 4 H) , 7.73 (d, J = 6.8 Hz, 1 H) , 7.45-7.43 (m, 2 H), 6.79 (s, 2 H), 5.01 (s, 2 H), 3.66 (t, J = 7.2 Hz, 2 H), 2.68 (t, J = 7.2 Hz, 2 H), 2.33 - 2.29 (m, 4 H), 1.55 - 1.45 (m, 2H), 1.40- 1.28 (M, 2 H) , 0.69 (t, J = 7.3, 6 H). FAB- MS: m/e = 445 (M + K) , 429 (M + Na), 407 (M + 1). The following phenoxyphenylacetic acid derivatives were prepared using the general procedures outlined in Example 5 . EXAMPLE 6 2-[(2,6-Dipropyl-4-(2-hydroxyethyl)phenoxy]-2-(3,4-methylenedioxyphenyl)acetic acid 1 H NMR (200 MHz, CD 3 OD, ppm): δ 7.03 (s, 1H), 6.83 (m, 3H), 6.72 (d, 1H, J=7.8 Hz), 5.93 (s, 2H), 4.80 (s, 1H), 3.68 (t, 2H, J=7.1 Hz), 2.69 (t, 2H, J=7.1 Hz), 2.35 (t, 4H, J=7.9 Hz), 1.42 (m, 4H), 0.83 (t, 6H, J=7.3 Hz). FAB-MS m/e = 401 (M+1) EXAMPLE 7 2-[(2,6-Dipropyl-4(1,2-dihydroxyethyl)phenoxy)]-2-(2-naphthyl)acetic acid STEP A : 2,6-dipropyl-4-vinylphenol The title compound was prepared from t-butyldimethylsilyloxy-2,6-dipropyl-4-vinylbenzene (Step B, Example 5) by treatment with tetrabutylammonium fluoride in THF for a few hours. It was poured into ether/ethyl acetate mixture and washed with brine. After removal of the solvent the crude product was purified by flash column chromatography using ethyl acetate/hexane as eluent. 1 H NMR (400 MHz, CDCL 3 , ppm): δ 7.01 (s, 2 H), 6.55 (dd, J = 17.6 , J = 11.0 Hz, 1H), 5.55 (d, J = 17.6 Hz, 1 H), 5.06 (d, J = 11.0 Hz, 1 H), 2.64 (t, J = 7.7 Hz, 4 H), 1.65 - 1.60 (m, 4 H), 0.96 (t, J = 7.2 Hz 6 H). STEP B : Methyl 2-[(2,6-dipropyl-4-vinyl)phenoxy]-2-(2-naphthyl)acetate The title compound was prepared by alkylation of 2,6-dipropyl-4-vinyl phenol (Step A) with methyl 2-bromo-2-(2-naphthyl)acetate using the procedure for alkylation described in Step B of Example 1. 1 H NMR (400 MHz, CDCl 3 , ppm): δ 7.9 - 7.8 (m, 4 H), 7.68 (d, J = 6.7 Hz, 1H), 7.50 - 7.48 (m, 2 H), 7.02 (s, 2 H), 6.57 (dd J = 18.4, 10.8 Hz, 1 H), 5.61 (d, J = 18.4, 1 H), 5.26 (s, 1 H), 5.14 (d, J = 10.8, 1 H), 3.73 (s, 1 H), 2.38 - 2.34 (m, 4 H), 1.54 - 1.43 (m, 4 H), 0.74 (t, J = 7.33 Hz, 6 H). STEP C : Methyl 2-[(2,6-dipropyl-4-(1,2-dihydroxyethyl)phenoxy]-2-(2-naphthyl)acetate To a solution of 6 mg (0.024 mmol) of OsO4 and 31 mg (0.263 mmol) of N-methylmorpholine-N-oxide (NMO) in 3 mL of acetone and 2 drops of water was added 96 mg (0.239 mmol) of the product of Step B. After 90 minutes the reaction mixture was poured into a mixture of ether and water. The layers were separated and the aqueous layer was extracted twice with ether. The combined aqueous layers were washed with saturated sodium chloride, dried over anhydrous magnesium sulfate, filtered and concentrated. Purification by flash chromatography (silica gel, hexane / ethyl acetate 1:1) gave 63 mg of the title compound. 1 H NMR (400 MHz, CDCl 3 , ppm): δ 7.89 - 7.80 (m, 4 H), 7.67 (d, J = 8.4 Hz, 1 H), 7.50 - 7.48 (m, 2 H), 6.9 (s, 2 H), 5.25 (s, 1 H), 4.75-4.68 (m, 1 H), 3.72 (s, 3 H), 3.75 - 3.61 (m, 2 H), 2.38 - 2.34 (m, 4 H), 1.53 - 1.46 (m, 4 H), 0.25 - 0.71 (m, 6 H). STEP D : 2-[(2,6-Dipropyl-4-(1,2-dihydroxyethyl)phenoxy]-2-(2-naphthyl)acetic acid The title compound was prepared from the product of Step C by saponification with 1N aqueous KOH solution as described above. 1 H NMR (400 MHz, CD 3 OD, ppm): δ 7.84 - 7.71 (m, 5 H), 7.46 - 7.42 (m, 2 H), 6.96 (s, 2 H), 5.03 (s, 1 H), 4.55 (t, J = 7.2 Hz, 1 H), 3.54 (d, J = 7.2 Hz, 2 H), 2.34 (t, J = 7.9 Hz, 4 H), 1.51-1.30 (m, 4 H), 020 (t, J = 7.3 Hz, 6 H). EXAMPLE 8 2-[(2,6-Dipropyl-4-(1-hydroxypentyl)phenoxy]-2-(2-naphthyl)acetic acid STEP A : Methyl 2-[(2,6-dipropyl-4-formyl)phenoxy]-2-(2-naphthyl)acetate To a solution of 262 mg (0.645 mmol) of methyl 2-[(2,6-dipropyl-4-hydroxymethyl)phenoxy]-2-(2-naphthyl)acetate in 2 mL of methylene chloride was added 404 mg (0.968 mmol) of PDC. After 4 hours the reaction mixture was diluted with 20 mL of ether and filtered through a pad of florisil / celite and concentrated to give 235 mg of the title compound. 1 H NMR (400 MHz, CDCl 3 , ppm): δ 9.86 (s, H), 7.89-7.80 (m, 4 H), 7.65 (m, 1 H), 7.52 - 7.49 (m, 4 H), 5.35 (s, 1 H), 3.73 (s, 3 H), 2.47-2.43 (m, 4 H), 1.54-1.43 (m, 4 H), 0.77 (t, J = 7.3 Hz, 6 H). STEP B : Methyl 2-[(2,6-dipropyl-4-(1-hydroxypentyl)phenoxy]-2- ( 2-naphthyl)acetate To a solution of 56 mg (0.143 mmol) of the product of Step A in 1 mL of THF at -78 °C was added 0.075 mL (2.0 M in THF, 0.150 mmol) of n-butyl magnesium chloride. TLC analysis showed that the starting material remained unconsumed so 0.020 mL of n-butyl magnesium chloride was added. After 1 h the reaction mixture was diluted with saturated aqueous ammonium chloride solution and then extracted twice with ethyl acetate. The organic layers were dried over anhydrous sodium sulfate, filtered and concentrated. Purification by flash colunm chromatography (silica gel, hexane / ethyl acetate 6 : 1) gave 32 mg of the title compound. 1 H NMR (400 MHz, CDCl 3 , ppm): δ 7.89-7.82 (m, 4 H), 7.67 (m, 1 H), 7.49-7.47 (m, 2 H), 6.9 (s, 2 H), 5.26 (s, 1 H), 2.36 (t, J = 8.0 Hz, 4 H), 1.75-1.2 (m, 8 H), 0.86 (t, J = 7.2 Hz, 3 H), 0.72 (t , J = 7.3 Hz, 6 H). STEP C : 2-[(2,6-Dipropyl-4-(1-hydroxypentyl)phenoxy)]-2-naphthylacetic acid The title compound was prepared from the product of Step B by saponification with aqueous 1N KOH in methanol as described above. 1 H NMR (400 MHz, CD 3 OD, ppm): δ 7.84-7.72 (m , 5 H), 7.45 - 7.43 (m, 2 H), 6.91 (s, 2 H), 5.03 (s, 1 H), 4.45 (t, 1 H), 2.36 - 2.32 (m, 4 H), 1.75 -1.45 (m, 4 H), 1.35 -1.29 (m, 4 H), 0.87 (t, J = 7.2 Hz, 3 H), 0.70 (t, J = 7.2 Hz, 6 H). FAB-MS : m/e = 487 (M+ K), 469 (M + Na). EXAMPLE 9 (Reference) 2-[4-Carboxy-2,6-dipropyl)phenoxyl-2-phenylacetic acid STEP A: t-Butyl 2-[(4-carbomethoxy-2,6-dipropyl)phenoxy]-2-phenylacetate Methyl 2,6-dipropyl-4-hydroxybenzoate (1.5 g, 6.383 mmol) was refluxed with K 2 CO 3 (1.5 equiv) and t-butyl α-bromophenylacetate (2.4 g, 8.856 mmol) in acetone for 16 h. The reaction mixture was filtered through Celite, the filter cake was washed with acetone and the combined filtrate and washings were concentrated. The resulting crude oil was chromatographed (flash column) using silica gel and 10% ethyl acetate in hexane to give the titled compound (2.7 g). 1 H NMR (400 MHz, CD 3 OD, ppm): δ 7.665 (s, 2H), 7.443 (dd, 2H), 7.345 (dd, 3H), 5.019 (s, 1H), 3.851 (s, 3H), 2.49-2.335 (m, 4H), 1.63-1.4 (m, 4H), 1.364 (s, 9H), 0.803 (t, 6H). STEP B: t-Butyl 2-[(4-carboxy-2,6-dipropyl)phenoxy]-2-phenyl acetate Saponification of the above t-butyl 2-[(4-carbomethoxy-2,6-dipropyl)phenoxy]-2-phenylacetate (200 mg, 0.47 mmol) with 1N aqueous solution of LiOH in methanol gave the titled compound (125 mg). 1 H NMR (400 MHz, CD 3 OD, ppm): δ 7.66 (s, 2H), 7.5-7.4 (dd, 2H), 7.43-7.36 (dd, 3H) 4.88 (s, 1H), 2.5-2.35 (m, 4H), 1.63-1.33 (m, 4H), 1.38 (t, 9H), 0.83 (t, 6H). STEP C: 2-[(4-Carbomethoxy-2,6-dipropyl)phenoxy]-2-phenylacetic acid t-Butyl 2-[(4-carbomethoxy-2,6-dipropyl)phenoxy]-2-phenylacetate (Step A) (125 mg, 0.293 mmol) was treated with 3 mL of trifluoroacetic acid (TFA) in methylene chloride for 2 h. The volatiles were removed to give the titled compound (90 mg). 1 H NMR (400 MHz, CD 3 OD, ppm): δ 7.67 (s, 2H), 7.463-7.44 (m, 2H), 7.387-7.362 (m, 3H), 5.177 (s, 1H), 3.856 (s, 3H), 2.377 (t, 4H), 1.6 -1.366 (m, 4H), 0.773 (t, 6H). STEP D : 2-[4-Carboxy-2,6-dipropyl)phenoxyl-2-phenylacetic acid The product of Step C (70 mg, 0.19 mmol) was treated with 1N aqueous solution of LiOH in methanol. The reaction was monitored by TLC. When the starting material was completely consumed, the mixture was acidified at 0°C to pH 5 by addition of 1N HCl. The aqueous phase was extracted with ethyl acetate, dried over anhydrous magnesium sulfate and filtered. The filtrate was concentrated to yield the titled compound (25 mg). 1 H NMR (400 MHz, CD 3 OD, ppm): δ 7.68 (s, 2H), 7.52-7.45 (m, 2H), 7.43-7.365 (m, 3H), 5.175 (s, 1H), 2.43 (t, 4H), 1.64-1.4 (m, 4H), 0.83 (t, 6H). EXAMPLE 10 2-[(4-Carboxy-2,6-dipropyl)phenoxy]-2-[3,4-methylenedioxyphenyl] acetic acid The titled compound was prepared using procedures similar to that described in Example 9. 1 H NMR (200 MHz, CD 3 OD, ppm): δ 7.68 (s, 2H), 7.02 (d, 1H, J=1.6 Hz), 6.84 (m, 2H), 5.98 (s, 2H), 5.08 (s, 1H), 2.44 (t, 4H, J=7.9 Hz), 1.52 (m, 4H), 0.86 (t, 6H, J=7.3 Hz). FAB-MS m/e = 401 (M+1) EXAMPLE 11 N-(4-t-butylbenzenesulfonyl)-2-(4-methoxycarbonyl-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide Step A : Preparation of 2-(4-carbomethoxy-2-propylphenoxy)-3,4-methylenedioxyphenylacetic acid To ethyl 2-(4-carbomethoxy-2-propylphenoxy)-3,4-methylenedioxyphenylacetate (Step A of Example 56) (2.04 g, 5.10 mmol) in MeOH (40 mL) was added 5 N NaOH (8 mL). The rapid reaction was followed immediately by TLC to monitor mono deesterification. The reaction was quenched with 9 N HCl (4.5 mL) after loss of the ethyl ester and before methyl ester saponification. A saturated solution of NaHCO 3 was added to the reaction until it was basic and the MeOH was removed in vacuo. The residue was partitioned between Et 2 O and water collecting the product in the aqueous phase and removing impurities with the organic phase. The aqueous phase was then acidified with 9 N HCl (pH = 1) and the product extracted into EtOAc. The solution was dried over MgSO 4 , filtered and the solvent removed, yield = 1.78 g (4.78 mmol, 94%) rf = 0.16 (80:10:1/CHCl 3 :MeOH:NH 4 OH). Step B : Preparation of the precursor sulfonamide To a dichloromethane solution of the sulfonyl chloride (leq) cooled to 0°C was added t-butylamine (3 eq). After 3-5 hrs the CH 2 Cl 2 was removed and replaced with EtOAc. The reaction solution was washed with 1 N HCl, water, 1 N NaOH and brine. The resulting solution was dried over MgSO 4 and filtered. The solvent was removed. To the resulting solid was added a couple of drops of anisole and then TFA to remove the t-butyl group. After all of the sulfonamide had been deprotected, the TFA was removed in vacuo and the residue taken up in EtOAc/Et 2 O. The solution was washed with saturated NaHCO 3 solution to remove any residual TFA, then with brine, dried over MgSO 4 , filtered and the solvent removed. The sulfonamide precursors used in the preparation of the compounds of Examples 14, 15, 17, 18, 23 and 24 were prepared from the corresponding sulfonyl chlorides utilizing the procedure described above. The sulfonamide precursors used in the preparation of the compounds of Examples 12 and 19-22 are commercially available. The sulfonamide precursors used in Examples 13, 16 and 18, whose sulfonyl chlorides are not commercially available, were prepared using standard chemistry: Preparation of precursor sulfonamide for Example 13 The t-butylsulfonamide of 4-bromobenzenesulfonyl chloride was prepared using the procedure described above. The t-butylsulfonamide was then coupled to phenylboronic acid in a palladium catalyzed cross-coupling reaction with NaOH, EtOH, toluene, and Pd(PPh 3 ) 4 at 100° C to afford the biphenylsulfonamide. Deprotection of the t-butylsulfonamide with TFA and anisole yielded the free sulfonamide. Preparation of precursor sulfonamide for Example 16 The t-butylsulfonamide of 2-thiophenesulfonyl chloride was prepared using the procedure described above. Treatment of the t-butylsulfonamide with BuLi then isobutyl iodide afforded the 5-isobutyl-2-thiophene-t-butylsulfonamide which was then deprotected with TFA and anisole to yield the free sulfonamide. Preparation of precursor sulfonamide for Example 18 The t-butylsulfonamide of p-nitrobenzenesulfonyl chloride was prepared using the procedure described above. Reduction of the nitro group to the amine was accomplished with hydrogen in MeOH over Pd-C. Treatment of the free amine with LiBr and (MeO) 3 PO and then NaOH afforded the dimethylamine and the t-butylsulfonamide was deprotected with TFA and anisole to yield the free sulfonamide. Step C : Preparation of N-(4-t-butylbenzenesulfonyl)-2-(4-carbomethoxy-2-propylphenoxy)-3,4-methylenedioxyphenylacetamide To the product of Step A (57.2 mg, 0.154 mmol) in dry THF (0.75 mL) was added CDI (76.0 mg, 0.469 mmol) and the reaction heated to 50°C for 2.5 hr. To this solution was added a solution of p-t-butylphenyl-sulfonamide (131.7 mg, 0.618 mmol) and DBU (92.1 µL, 0.594 mmol) in dry THF (0.75 mL). The reaction continued to be stirred at 50°C monitoring by thin layer chromatography until all of the mono-acid was consumed (approx. 3 hr). The reaction was concentrated in vacuo and the residue was taken up in 50:50/Et 2 O:EtOAc. The organic phase was washed with 10% citric acid (2x), water and brine then dried over MgSO 4 , filtered and the solvent removed. Purification was accomplished by radial chromatography eluting wit 3:2/Hex:EtOAc. yield = 74.3 mg (0.131 mmol, 85%) rf = 0.32 (80:10:1/CHCl 3 :MeOH:NH 4 OH) FAB mass spectrum, m/e 590.0 (M+Na calculated for C 30 H 33 NSO 8 590). See Drummond, J.T.; Johnson, G. Tetrahedron Lett., 1988 , 29 , 1653. EXAMPLES 12-24 Examples 12 through 24 were prepared following the procedures described above in Example 11. Ex.# Z Mass Spectrum 12 CONHSO 2 Ph (M+1) 512.0 13 CONHSO 2 -(p-phenyl)Ph (M+Na) 610.0 14 CONHSO 2 -(p-Cl)Ph (M+) 546.0 15 CONHSO 2 -(p-Me)Ph 16 CONHSO 2 -(5-iBu)thiophene (M+Na) 596.4 17 CONHSO 2 -(p-MeO)Ph (M+1) 542.0 18 CONHSO 2 -(p-NMe 2 )Ph (M+1) 555.1 19 CONHSO 2 -(o-Me)Ph (M+1) 526.1 20 CONHSO 2 -(o-CO 2 Me)Ph (M+) 570.0 21 CONHSO 2 -(o-Cl)Ph (M+) 546.0 22 CONHSO 2 -(m-Cl)Ph (M+) 546.0 23 CONH-dansyl (M+1) 605.1 24 CONHSO 2 -8-quinoline (M+1) 563.4 The proton NMR data for Example 15 is given below: EXAMPLE 15 N-(4-methylbenzenesulfonyl)-2-(4-methoxycarbonyl-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide 1 H NMR (400 MHz, CD 3 OD, ppm): δ 0.89 (t, 3H), 1.59 (m, 2H), 2.34 (s, 3H), 2.63 (m, 2H), 3.85 (s, 3H), 5.49 (s, 1H), 5.97 (s, 2H), 6.55 (d, 1H), 6.79 (d, 1H), 6.91 (d, 1H), 6.96 (dd, 1H), 7.26 (d, 2H), 7.58 (dd, 1H), 7.70 (d, 2H), 7.74 (d, 1H). EXAMPLE 25 N-(4-t-butylbenzenesulfonyl)-2-(4-carboxy-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide To the product of Example 11 (51.1 mg, 0.090 mmol) in MeOH (2 mL) was added 5 N NaOH (0.5 mL). The reaction was monitored by TLC. When the reaction was complete the MeOH was removed and the residue partitioned between water and Et 2 O:EtOAc. The water layer was acidified with HCl solution and the product extracted into the organic phase. The organic phase was washed with brine then dried over MgSO 4 , filtered and the solvent removed. Trituration with Et 2 O/Hex provided a white solid, yield = 25.8 mg (0.047 mmol, 52%) FAB mass spectrum, m/e 554.2 (M+1 calculated for C 29 H 31 NSO 8 554). EXAMPLES 26-38 Examples 26 through 38 were prepared following the procedures described above in Example 25. Ex. # Z Mass Spectrum 26 CONHSO 2 Ph (M+1) 498.0 27 CONHSO 2 -(p-phenyl)Ph (M+) 573.5 28 CONHSO 2 -(p-Cl)Ph (M+) 532.0 29 CONHSO 2 -(p-Me)Ph (M+K) 549.9 30 CONHSO 2 -(5-iBu)thiophene (M+Na) 582.0 31 CONHSO 2 -(p-MeO)Ph (M+1) 528.0 32 CONHSO 2 -(p-NMe 2 )Ph (M+1) 541.1 33 CONHSO 2 -(o-Me)Ph (M+1) 512.0 34 CONHSO 2 -(o-CO 2 H)Ph (M+1) 542.1 35 CONHSO 2 -(o-Cl)Ph (M+1) 532.2 36 CONHSO 2 -(m-Cl)Ph (M+1) 532.4 37 CONH-dansyl (M+1) 591.0 38 CONHSO 2 -8-quinoline (M+1) 549.2 The proton NMR data for several of the Examples is given below: EXAMPLE 32 N-(4-dimethylaminobenzenesulfonyl)-2-(4-carboxy-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide 1 H NMR (300 MHz, CD 3 OD, ppm): δ 0.89 (t, 3H), 1.59 (m, 2H), 2.62 (m, 2H), 3.03 (s, 6H), 5.48 (s, 1H), 5.96 (s, 2H), 6.43 (d, 1H), 6.64 (dd, 2H), 6.79 (d, 1H), 6.91 (m, 2H), 7.55 (dd, 1H), 7.64 (dd, 2H), 7.74 (d, 1H). EXAMPLE 34 N-(2-carboxybenzenesulfonyl)-2-(4-carboxy-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide 1 H NMR (400 MHz, CD 3 OD, ppm): δ 0.92 (t, 3H), 1.62 (m, 2H), 2.67 (m, 2H), 5.66 (s, 1H), 5.95 (s, 2H), 6.74 (d, 1H), 6.77 (d, 1H), 6.93 (d, 1H), 6.98 (dd, 1H), 7.60 (m, 2H), 7.69 (m, 1H), 7.75 (m, 2H), 8.09 (d, 1H). EXAMPLE 37 N-(dansylsulfonyl)-2-(4-carboxy-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide 1H NMR (400 MHz, CD 3 OD, ppm): δ 0.83 (t, 3H), 1.51 (m, 2H), 2.57 (m, 2H), 2.88 (s, 6H), 5.40 (s, 1H), 5.95 (dd, 2H), 6.26 (d, 1H), 6.65 (d, 1H), 6.79 (d, 1H), 6.85 (dd, 1H), 7.19 (dd, 1H), 7.25 (d, 1H), 7.48 (t, 1H), 7.54 (t, 1H), 7.66 (d, 1H), 8.13 (d, 1H), 8.30 (dd, 1H), 8.53 (d, 1H). EXAMPLE 38 N-(8-quinolinesulfonyl)-2-(4-carboxy-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide 1 H NMR (300 MHz, CD 3 OD, ppm): δ 0.85 (t, 3H), 1.54 (m, 2H), 2.59 (m, 2H), 5.57 (s, 1H), 5.94 (s, 2H), 6.47 (d, 1H), 6.66 (d, 1H), 6.71 (d, 1H), 6.87 (dd, 1H), 7.34 (dd, 1H), 7.58 (dd, 1H), 7.68 (m, 2H), 8.20 (dd, 1H), 8.39 (dd, 1H), 8.47 (dd, 1H), 8.83 (dd, 1H). EXAMPLE 39 N-(8-quinolinesulfonyl)-2-(4-carboxamido-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide To N-(8-quinolinesulfonyl)-2-(4-carboxy-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide, Example 38, (25.8 mg, 0.047 mmol) in dry DMF (0.5 mL) was added 1-(3-dimethylaminopropyl)-3-ethylcarbodiimide hydrochloride, also referred to as EDC, (18.4 mg, 0.096 mmol), NH 4 Cl (6.7 mg, 0.125 mmol), and TEA (17.5 mL, 0.125 mmol). Reaction was followed by thin layer chromatography (100:15:1.5/CH 2 Cl 2 :MeOH:HOAc). When the reaction was completed the DMF was removed in vacuo and the residue taken up in Et 2 O/EtOAc. The solution was washed with 10% citric acid, water and brine then dried over MgSO 4 , filtered and the solvent removed. The product was purified by chromatography eluting with 200:5:1.5/CH 2 Cl 2 :MeOH:HOAc. rf = 0.35 (100:5:1.5/CH 2 Cl 2 :MeOH:HOAc) FAB mass spectrum, m/e 548.0 (M+1 calculated for C 28 H 25 N 3 SO 7 548). EXAMPLE 40 α-(4-carbomethoxy-2- n -propylphenoxy)-3,4-methylenedioxyphenyl)acetic acid Step A: Preparation of ethyl α-(4-carbomethoxy-2- n -propylphenoxy)-3,4-methylenedioxyphenylacetate To a 2 L three necked 24/40 round bottom flask equipped with a mechanical stirrer, a nitrogen inlet and a dropping funnel was first added a solution of 36.0 g (0.185 mol) of methyl 4-hydroxy-3- n -propylbenzoate dissolved in 700 mL of anhydrous DMF followed by 66.4 g (0.204 mol) of cesium carbonate. The flask was purged with nitrogen and the reaction mixture was stirred at room temperature for 2 hours. A solution of 58.5 g (0.204 mol) of ethyl α-bromo-3,4-methylenedioxyphenylacetate dissolved in 100 mL of DMF was then added via an addition funnel over a 15 minute period. The reaction mixture was stirred an additional 1 hour at room temperature then quenched by addition to 5 L of a 5% aqueous citric acid solution. The organic product was extracted into diethylether (2 x 4 L), the organic layers were separated, washed with saturated aqueous NaCl, dried (MgSO 4 ), filtered, and evaporated. The residue was applied to a silica gel (2 kg; 70-230 mesh) column equillibrated in 10% CH 2 Cl 2 -hexane. The column was then eluted successively with 12 L of 10% CH 2 Cl 2 -hexane, 12 L of 5% EtOAc-hexane, 4 L of 7.5% EtOAc-hexane, 12 L of 10% EtOAc-hexane, and finally 8 L of 20% EtOAc-hexane. Combination of the purified fractions and evaporation in vacuo afforded 76.3 g (74.2 theoretical) of the title compound as a pale yellow oil which was used without further purification in the next step. Step B: Preparation of α-(4-carbomethoxy-2- n -propylphenoxy)-3,4-methylenedioxyphenylacetic acid A 1 L 3 necked 24/40 round bottom flask equipped with a mechanical stirrer, a dropping funnel, and a nitrogen inlet was charged with a solution of 76.3 g 0.185 mol) of the semi-purified product of Step A dissolved in 500 mL of methanol. The flask was purged with nitrogen, the stirrer was started, and 37 mL of a 5.0 N aqueous solution of sodium hydroxide was added over a 30 minute period via an addition funnel. The reaction mixture was stirred at room temperature for an additional 30 minutes at which point TLC analysis (CH 2 Cl 2 -MeOH-NH 4 OH 90:10:1) indicated that the starting material had been consumed. The reaction mixture was adjusted to pH=4 with 6 N HCl, and the bulk of the organic solvent was removed in vacuo. The precipitated organic product and the aqueous layer were next partitioned between CH 2 Cl 2 (1 L) and water (1 L) which produced a copious emulsion. The reaction mixture was then aged overnight in a refridgerator which resulted in crystallization of the organic product. The crystalline solid was separated from the two phase mixture by filtration and washed with CH 2 Cl 2 . The solid was slurried again in diethylether, filtered, washed with hexane, and then dried in a vacuum to afford 65 g (94%) of the title compound as a white crystalline solid. 1 H-NMR (400 MHz, CD 3 OD, ppm): δ 0.93 (t, J =7.20 Hz, 3H), 1.62-1.75 (m, 2H), 2.63-2.70 (m, 1H), 2.77-2.81 (m, 1H), 3.84 (s, 3H), 5.54 (s, 1H), 5.94 (s, 2H), 6.81 (d, J =7.60 Hz, 1H), 6.89 (d, J =9.20 Hz, 1H), 7.08 (d, J =1.60 Hz, 1H), 7.11 (br s, 1H), 7.78-7.81 (m, 2H). EXAMPLE 41 N -(4- iso -propylbenzenesulfonyl)-α-(4-carbomethoxy-2- n -propylphenoxy)-3,4-methylenedioxyphenylacetamide Step A: Preparation of N -(4- iso -propylbenzenesulfonyl)-α-(4-carbomethoxy-2- n -propylphenoxy)-3,4-methylenedioxyphenylacetamide An oven dried three-necked 24/40 1 L round-bottom flask was equipped with a mechanical stirrer, a nitrogen inlet, and a septum. The flask was flushed with nitrogen, then charged wit 20.06 g (53.9 mmol) of the product of Example 40, 400 mL of anhydrous THF, and 9.76 mL (70.0 mmol) of triethylamine. The flask and its contents were stirred and cooled to -78°C with an external dry ice-acetone bath and then 7.30 mL (59.3 mmol) of trimethylacetyl chloride was added slowly via a syringe. After the addition was complete, the dry ice-acetone bath was replaced with an ice-water bath and the reaction was stirred at 0°C for 1 hour. A separate oven dried 3 necked 24/40 2 L round-bottom flask was equipped with a mechanical stirrer, a septum and a nitrogen inlet. The flask was flushed with nitrogen then charged with 16.102 g (80.8 mmol) of 4- iso -propylbenzenesulfonamide and 300 mL of anhydrous methyl sulfoxide. The stirrer was started and a 162 mL of a 1.0 M solution of lithium bis(trimethylsilylamide) in THF was slowly (mildly exothermic) added via a syringe trough the septum. After the addition was complete, the reaction mixture was stirred at room temperature for an additional 30 minutes. The contents of the first reaction mixture including a fine white precipitate that was suspended in the reaction mixture were then slowly transfered to the stirred solution of the deprotonated sulfonamide in the second flask via a wide diameter cannula. The combined reaction mixture was then stirred for an additional 14 hours under a nitrogen atmosphere. The reaction was the quenched with 1.0 N HCl and the majority of the volatile solvents were removed in vacuo. The residue was partitioned between EtOAc and 1.0 N HCl, then organic layer was separated, washed with saturated aqueous NaCl, dried (MgSO 4 ), filtered and evaporated in vacuo. The residue was purified on a silica gel (3 kg; 70-230 mesh) chromatography column (15 cm x 150 cm) eluted with (90:10:1 CH 2 Cl 2 -MeOH-NH 4 OH). Combination of the purified fractions and evaporation in vacuo afforded 18.367 g (62%) of the title compound. 1 H-NMR (400 MHz, CD 3 OD, ppm): δ 0.88 (t, J =7.60 Hz, 3H), 1.24 (d, J =7.00 Hz, 3H), 1.25 (t, J =7.00 Hz, 3H), 1.55-1.60 (m, 2H), 2.59-2.66 (m, 2H), 2.97 (sept, J =7.00 Hz, 1H), 3.83 (s, 3H), 5.52 (s, 1H), 5.97 (s, 2H), 6.50 (d, J =8.80 Hz, 1H), 6.80 (d, J =8.00 Hz, 1H), 6.89 (d, J =1.60 Hz, 1H), 6.94 (dd, J =2.00, 8.00 Hz, 1H), 7.14 (d, J =8.80 Hz, 2H), 7.59 (dd, J =2.20, 8.80 Hz, 1H), 7.75 (d, J =2.20, 1H), 7.79 (d, J =8.80 Hz, 2H). EXAMPLE 42 N -(4- iso -propylbenzenesulfonyl)-α-(4-carboxy-2- n -propylphenoxy)-3,4-methylenedioxyphenylacetamide dipotassium salt Step A: Preparation of N -(4- iso -propylbenzenesulfonyl)-α-(4-carboxy-2- n -propylphenoxy)-3,4-methylenedioxyphenylacetamide dipotassium salt To a solution of 18.367 g (33.2 mmol) of the product of Example 41 dissolved in 100 mL of methanol was added a solution of 6.56 g (116.9 mmol) of potassium hydroxide in 25 mL of water and the reaction mixture was stirred at 60°C under a nitrogen atmosphere. After 6 hours TLC analysis (80:15:1 CHCl 3 -MeOH-NH 4 OH) indicated that ester hydrolysis was complete. The reaction mixture was cooled to room temperature, diluted with 100 mL water, filtered through a 0.45 micron filter and then divided into two equal volume portions. The fractions were individually desalted and purified on a Waters Millipore Delta Prep 3000 liquid chromatograph equipped with an M1000 PrepPak module containing a 47 x 300 mm Delta-Pak C18 15µm 100A column cartridge. Two solvent resevoirs were employed: solvent system A (95-5 water-acetonitrile), and solvent system B (5-95 water-acetonitrile), and the column effluent was monitored simultaneously at 210 and 280 nm with a Waters model 490 UV-visible detector. Each fraction was pump-injected onto the column and desalted by elution (50 mL/min) with several column volumes of solvent system A. A gradient elution was then begun which had as initial conditions 100% solvent system A-0% solvent system B and reached after 30 minutes 50% solvent system A-50% solvent system B, and the fractions were collected with an ISCO Foxy 200 fraction collector. The purified fractions were combined in round bottom flasks, frozen in a -78°C dry ice-acetone bath, and lyophilized. Combination of the purified product afforded 18.719 g (92%) of the title compound as a white lyophilized powder. 1 H-NMR (400 MHz, CD 3 OD, ppm): δ 0.88 (t, J =7.20 Hz, 3H), 1.21 (d, J =7.00 Hz, 3H), 1.22 (d, J =7.00 Hz, 3H), 1.56-1.63 (m, 2H), 2.52-2.59 (m, 1H), 2.67-2.74 (m, 1H), 2.91 (sept, J =7.00 Hz, 1H), 5.33 (s, 1H), 5.92 (d, J =1.20 Hz, 1H), 5.93 (d, J =1.20 Hz, 1H), 6.72 (d, J =8.50 Hz, 1H), 6.76 (d, J =8.50 Hz, 1H), 7.04 (d, J =7.50 Hz, 1H), 7.05 (s, 1H), 7.21 (d, J =8.50 Hz, 2H), 7.64 (dd, J=2.00, 8.50 Hz, 1H), 7.67 (d, J =8.50 Hz, 2H), 7.73 (d, J =2.00 Hz, 1H). Microanalysis for C 28 H 27 NSO 8 K 2 ·H 2 O. Calc'd: C = 53.06; H = 4.61; N = 2.21; K = 12.34. Found: C = 52.81; H = 4.56; N = 2.17; K = 12.02. EXAMPLE 43 α-(2- iso -butyl-4-carbomethoxyphenoxy)-3,4-methylenedioxyphenylacetic acid Step A: Preparation of ethyl α-(2- iso -butyl-4-carbomethoxyphenoxy)-3,4-methylenedioxyphenylacetate To a solution of 1.008 g (4.84 inmol) of methyl 3- iso butyl-4-hydroxybenzoate and 1.737 g (6.05 mmol) of ethyl α-bromo-3,4-methylenedioxyphenylacetate in 10 mL of acetone was added 1.338 g (10 mmol) of finely powdered potassium carbonate. The reaction mixture was magnetically stirred and refluxed for 4 hours, then cooled to room temperature, filtered and evaporated. The residue was purified on a silica gel flash chromatography column eluted with 10% EtOAc-hexane; combination of the purified fractions and drying in vacuo afforded 1.518 g (76%) of the title compound as an amorphous powder. 1 H-NMR (400 MHz, CDCl 3 , ppm): δ 0.90 (d, J =6.60 Hz, 3H), 0.94 (d, J =6.60 Hz, 3H), 1.17 (t, J =7.20 Hz, 3H), 2.02-2.08 (m, 1H), 2.55 (dd, J =7.20, 13.20 Hz, 1H), 2.64 (dd, J =7.20, 13.20 Hz, 1H), 3.85 (s, 3H), 4.11-4.19 (m, 2H), 5.56 (s, 1H), 5.96 (s, 2H), 6.70 (d, J =9.20 Hz, 1H), 6.68 (d, J =7.60 Hz, 1H), 7.02 (dd, J =1.60, 8.00 Hz, 1H), 7.05 (d, J =2.00 Hz, 1H), 7.78-7.81 (m, 2H). Step B: Preparation of α-(2- iso -butyl-4-carbomethoxyphenoxy)-3,4-methylenedioxyphenylacetic acid To a solution of 1.518 g ( 3.66 mmol) of the product of Step A dissolved in 8.0 mL of methanol was added 1.0 mL of a 5.0 M solution of aqueous sodium hydroxide. The reaction was stirred at room temperature and monitored by TLC (80:15:1 CHCl 3 -MeOH-NH 4 OH). After 1.5 hours the reaction was judged to be complete and the reaction mixture was adjusted to pH=5 with 1.0 N HCl. The reaction mixture was then partitioned between EtOAc and water, separated, dried (MgSO 4 ), filtered, and evaporated. The residue was purified on a silica gel flash chromatography column eluted with CHCl 3 -MeOH-NH 4 OH (80:15:1); evaporation of the purified fractions and drying in vacuo afforded the title compound as an amorphous foam. 1 H-NMR (400 MHz, CD 3 OD, ppm): δ 0.86 (d, J =6.80 Hz, 3H), 0.89 (d, J =6.80 Hz, 3H), 1.96-2.04 (m, 1H), 2.49 (dd, J =7.20, 12.80 Hz, 1H), 2.69 (dd, J =7.20, 12.80 Hz, 1H), 3.84 (s, 3H), 5.49 (s, 1H), 5.92 (d, J =1.20 Hz, 1H), 5.93 (d, J =1.20 Hz, 1H), 6.79 (d, J =8.00 Hz, 1H), 6.89 (d, J =8.80 Hz, 1H), 7.08 (dd, J =1.60, 8.00 Hz, 1H), 7.11 (d, J =1.60 Hz, 1H), 7.74 (d, J =2.40 Hz, 1H), 7.78 (dd, J =2.40, 8.80 Hz, 1H). CI-MS m/e = 386.2 (M + ). EXAMPLE 44 N -(4- iso -propylbenzenesulfonyl)-α-(2- iso -butyl-4-carbomethoxyphenoxy)-3,4-methylenedioxyphenylacetamide Step A : Preparation of N -(4- iso -propylbenzenesulfonyl)-α-(2- iso -butyl-4-carbomethoxyphenoxy)-3,4-methylenedioxyphenylacetamide To a solution of 0.727 g (1.88 mmol) of the product of Step B in Example 42 dissolved in 4 mL of anhydrous THF was added 0.458 g (2.82 mmol) of 1,1'-carbonyldiimidazole and the mixture was magnetically stirred and refluxed for 2 hours. The reaction mixture was then cooled to room temperature, and 0.562 g (2.82 mmol) of 4- iso -propylbenzenesulfonamide and 0.42 mL (2.82 mmol) of 1,8-diazabicyclo[5.4.0]undec-7-ene were added. The reaction mixture was stirred an additional 3 hours at room temperature, then was evaporated in vacuo. The residue was partitioned between EtOAc and 1.0 N HCl and extracted. The organic layer was separated, dried (MgSO 4 ), filtered, and evaporated and the residue was purified on a silica gel flash chromatography column eluted with CHCl 3 -MeOH-NH 4 OH (80:15:1). Evaporation of the purified fractions and drying in vacuo afforded 0.666 g (63%) of the title compound. 1 H-NMR (400 MHz, CD 3 OD, ppm): δ 0.81 (d, J =6.80 Hz, 3H), 0.84 (d, J =6.80 Hz, 3H), 1.23 (d, J =6.80 Hz, 3H), 1.24 (d, J =6.80 Hz, 3H), 1.88-1.94 (m, 1H), 2.45 (dd, J =7.00, 13.00 Hz, 1H), 2.58 (dd, J =7.00, 13.00 Hz, 1H), 2.95 (sept, J =6.80 Hz, 1H), 3.84 (s, 3H), 5.46 (s, 1H), 5.95 (d, J =1.20 Hz, 1H), 5.96 (d, J =1.20 Hz, 1H), 6.59 (d, J =8.60 Hz, 1H), 6.79 (d, J =8.00 Hz, 1H), 6.98 (br s, 1H), 6.99 (dd, J =1.60, 8.00 Hz, 1H), 7.30 (d, J =8.40 Hz, 2H), 7.60 (dd, J =2.00, 8.60 Hz, 1H), 7.70 (d, J =2.00 Hz, 1H), 7.72 (d, J =8.40 Hz, 2H). EXAMPLE 45 N -(4- iso -propylbenzenesulfonyl)-α-(2- iso -butyl-4-carboxyphenoxy)-3,4-methylenedioxyphenylacetamide Step A: Preparation of N -(4- iso -propylbenzenesulfonyl)-α-(2- iso -butyl-4-carboxyphenoxy)-3,4-methylenedioxyphenylacetamide To a solution of 0.294 g (0.52 mmol) of the product of Example 44 dissolved in 3.0 mL of methanol was added 1.0 mL of a 5.0 N aqueous solution of sodium hydroxide. The reaction mixture was magnetically stirred at 60°C. After 3 hours TLC analysis (CHCl 3 -MeOH-NH 4 OH 80:15:1) indicated complete hydrolysis of the ester. The reaction was cooled to room temperature, adjusted to pH=5 with dropwise addition of 1.0 N HCl, then partitioned between EtOAc and water. The organic layer was separated, washed with saturated aqueous NaCl, dried (MgSO 4 ), filtered and evaporated. The residue was dried in vacuo to afford 0.238 g (83%) of the title compound as an amorphous powder. 1 H-NMR (400 MHz, CD 3 OD, ppm): δ 0.82 (d, J =6.80 Hz, 3H), 0.85 (d, J =6.80 Hz, 3H), 1.24 (d, J =7.20 Hz, 3H), 1.25 (d, J =7.20 Hz, 3H), 1.91 (sept, J =6.80 Hz, 1H), 2.48 (dd, J =7.20, 13.20 Hz, 1H), 2.56 (dd, J =7.20, 13.20 Hz, 1H), 2.97 (sept, J =7.20 Hz, 1H), 5.51 (s, 1H), 5.97 (s, 1H), 6.50 (d, J =8.40 Hz, 1H), 6.81 (d, J =8.00 Hz, 1H), 6.91 (d, J =1.60 Hz, 1H), 6.95 (dd, J =1.60, 8.00 Hz, 1H), 7.36 (d, J =8.40 Hz, 2H), 7.62 (dd, J =2.20, 8.40 Hz, 1H), 7.72 (d, J =2.20 Hz, 1H), 7.79 (d, J =8.40 Hz, 2H). FAB-MS m/e = 554 (M + 1). EXAMPLE 46 N -(4- iso -propylbenzenesulfonyl)-α-(2- n -propyl-4-carboxamidophenoxy)-3,4-methylenedioxyphenylacetamide Step A: Preparation of N -(4- iso -propylbenzenesulfonyl)-α-(2- n -propyl-4-carboxamidophenoxy)-3,4-methylenedioxyphenylacetamide To a solution of 0.162 g (0.30 mmol) of N -(4- iso -propylbenzenesulfonyl)-α-(4-carboxy-2- n -propylphenoxy)-3,4-methylenedioxyphenylacetamide (free acidic form of the product of Example 42) dissolved in 1.5 mL of anhydrous THF was added 0.073 g (0.45 mmol) of 1,1'-carbonyldiimidazole and the resulting mixture was magnetically stirred and refluxed for 50 minutes. The reaction mixture was cooled to room temperature, and then added at 0°C to excess THF that had been previously saturated with anhydrous gaseous ammonia. The reaction mixture was sealed and then stirred at room temperature for 14 hours. The reaction mixture was then poured into water (70 mL) and extracted with EtOAc (150 mL). The organic layer was separated, washed with saturated aqueous NaCl, dried (MgSO 4 ), filtered, and evaporated in vacuo to afford the title compound as an amorphous solid. 1 H-NMR (400 MHz, CD 3 OD, ppm): δ 0.88 (t, J =7.60 Hz, 3H), 1.21 (d, J =6.80 Hz, 6H), 1.55-1.66 (m, 2H), 2.54-2.62 (m, 1H), 2.70-2.77 (m, 1H), 2.89 (sept, J =6.80 Hz, 1H), 5.36 (s, 1H), 5.93 (d, J =1.20 Hz, 1H), 5.94 (d, J =1.20 Hz, 1H), 6.75 (d, J =8.40 Hz, 1H), 6.78 (d, J =8.80 Hz, 1H), 7.02-7.04 (m, 2H), 7.06 (br s, 2H), 7.20 (d, J =8.40 Hz, 2H), 7.55 (dd, J =2.20, 8.60 Hz, 1H), 7.62-7.66 (m, 2H), 7.71 (s, 1H). FAB-MS m/e = 539 (M + 1). EXAMPLE 47 N -(4- iso -propylbenzenesulfonyl)-α-(2- n -propyl-4-hydroxymethylphenoxy)-3,4-methylenedioxyphenylacetamide Step A: Preparation of methyl α-(4-hydroxymethyl-2- n -propylphenoxy)-3,4-methylenedioxyphenylacetate To a solution of 3.84 g (23.13 mmol) of 4-hydroxy-3- n -propylbenzyl alcohol dissolved in 70 mL of anhydrous DMF was added 9.04 g (27.7 mmol) of cesium carbonate and the reaction mixture was magnetically stirred at room temperature for 15 minutes. Methyl α-bromo-3,4-methylenedioxyphenylacetate (7.58 g; 27.7 mmol) was added and the reaction mixture was then stirred for an additional 14 hours at room temperature under a nitrogen atmosphere. The reaction was then partitioned between 5% aqueous citric acid (700 mL) and EtOAc (100 mL) and extracted. The organic layer was separated, washed with saturated aqueous NaCl, dried (MgSO 4 ), filtered and evaporated. The residue was purified on a silica gel flash chromatography column eluted with 40% EtOAc-hexane. The purified fractions were combined, evaporated, and dried in vacuo to afford 6.74 g (81 %) of the title compound as a yellow oil. 1 H-NMR (200 MHz, CDCl 3 , ppm): δ 0.97 (t, J =7.60 Hz, 3H), 2.55-2.75 (m, 2H), 2.71 (t, J =7.20 Hz, 2H), 3.71 (s, 3H), 4.59 (s, 2H), 5.55 (s, 1H), 5.97 (s, 2H), 6.69 (d, J =8.20 Hz, 1H), 6.82 (d, J =7.80 Hz, 1H), 7.02-7.28 (m, 4H). FAB-MS m/e = 359 (M + 1). Step B: Preparation of methyl α-(4- tert -butyldimethylsilyloxymethyl-2- n -propylphenoxy)-3,4-methylenedioxyphenylacetate To a solution of 2.50 g (6.98 mmol) of the product of Step A dissolved in 20 mL of dichloromethane was added 1.95 mL (14.0 mmol) of triethylamine, 1.26 g (8.38 mmol) of tert -butyldimethylchlorosilane, 85 mg (0.1 eq) of 4-dimethylaminopyridine and the reaction mixture was stirred at room temperature for 30 minutes under a nitrogen atmosphere. The reaction was then diluted with 100 mL EtOAc, washed with water, 1.0 N HCl, saturated aqueous NaHCO 3 , saturated NaCl, dried (MgSO 4 ), filtered and evaporated in vacuo to afford 3.20 g (97%) of the title compound. EI-MS m/e = 472 (M + ). Step C : Preparation of α-(4- tert -butyldimethylsilyloxymethyl-2- n -propylphenoxy)-3,4-methylenedioxyphenylacetic acid To a solution of 3.20 g (6.78 mmol) of the product of Step B dissolved in 10 mL of methanol and 3 mL of dichloromethane was added 1.42 mL (7.12 mmol) of a 5.0 N aqueous solution of sodium hydroxide and the reaction mixture was magnetically stirred at room temperature. After 4 hours TLC analysis (CHCl 3 -MeOH-NH 4 OH 80:15:1) indicated complete hydrolysis and the reaction mixture was adjusted to pH=4 with 1.0 N HCl. The reaction mixture was then completely evaporated and dried in vacuo to afford the crude product which was used directly in the next step. FAB-MS m/e = 481 (M + Na + ). Step D: Preparation of N -(4- iso -propylbenzenesulfonyl)-α-(4- tert -butyldimethylsilyloxymethyl-2- n -propylphenoxy)-3,4-methylenedioxyphenylacetamide To a solution of 3.30 g (7.21 mmol) of the crude product from Step C dissolved in 40 mL of anhydrous THF was added 1.75 g (10.8 mmol) of 1,1'-carbonyldiimidazole and the reaction mixture was magnetically stirred and heated at reflux for 10 minutes. The reaction was then cooled to room temperature, 2.15 g (10.8 mmol) of 4- iso -propylbenzenesulfonamide and 1.61 mL (10.8 mmol) of 1,8-diazabicyclo[5.4.0]undec-7-ene were added and the reaction was stirred for an additional 30 minutes at room temperature. The mixture was then diluted with EtOAc (80 mL), washed with 10% aqueous citric acid, saturated aqueous NaCl, dried (MgSO 4 ), filtered and evaporated. The residue was partially purified on a silica gel flash chromatography column eluted with CHCl 3 -MeOH-NH 4 OH (92:8:0.5). The semi-purified material was combined and repurified on a second silica gel flash chromatography column eluted initially with 35% EtOAc-hexane, later with 50% EtOAc-hexane, and finally with 70% EtOAc-hexane. Combination of the purified fractions and evaporation afforded 3.20 g (69%) of the title compound as a yellow oil. FAB-MS m/e = 678 (M + K + ). Step E : Preparation of N -(4- iso -propylbenzenesulfonyl)-α-(4-hydroxymethyl-2- n -propylphenoxy)-3,4-methylenedioxyphenylacetamide To a solution of 3.20 g (5.01 mmol) of the product of Step D dissolved in 5.0 mL of anhydrous THF was added 5.06 mL (5.06 mmol) of a 1.0 M solution of tetrabutylammonium fluoride in THF and the reaction mixture was stirred at room temperature under a nitrogen atmosphere. After 2.5 hours 1.0 mL additional tetrabutylammonium fluoride in THF was added and the reaction mixture was stirred for an additional 14 hours. The reaction mixture was then concentrated in vacuo and applied to a silica gel flash chromatography column and eluted with 60% EtOAc-hexane. Combination of the purified fractions and drying in vacuo afforded 0.691 g (26%) of the title compound as an amorphous powder. 1 H-NMR (400 MHz, CD 3 OD, ppm): δ 0.87 (t, J =7.60 Hz, 3H), 1.26 (d, J =6.80 Hz, 3H), 1.27 (d, J =6.80 Hz, 3H), 1.51-1.63 (m, 2H), 2.54-2.68 (m, 2H), 2.98 (sept, J =6.80 Hz, 1H), 4.46 (s, 2H), 5.37 (s, 1H), 5.95 (s, 1H), 6.51 (d, J =8.40 Hz, 1H), 6.77 (d, J =8.00 Hz, 1H), 6.88-6.95 (m, 3H), 7.10 (d, J =2.00 Hz, 1H), 7.36 (d, J =8.40 Hz, 2H), 7.77 (d, J =8.40 Hz, 2H). FAB-MS m/e = 548 (M + Na + ). EXAMPLE 48 α-(2- n -propylphenoxy)-3,4-methylenedioxyphenylacetic acid FAB-MS for C 18 H 18 O 5 : m/e = 337 (M + Na + ). EXAMPLE 49 N -(4- iso -propylbenzenesulfonyl)-α-(2- n -propylphenoxy)-3,4-methylenedioxyphenylacetamide FAB-MS for C 27 H 29 NSO 6 : m/e = 534 (M + K + ). EXAMPLE 50 α-(2-(2-hydroxyethyl)phenoxy)-3,4-methylenedioxyphenylacetic acid FAB-MS for C 17 H 16 O 6 : m/e = 317 (M + 1). EXAMPLE 51 α-(4-hydroxymethyl-2- n -propylphenoxy)-3,4-methylenedioxyphenylacetic acid CI-MS for C 19 H 20 O 6 : m/e = 326 (M + - H 2 O). EXAMPLE 52 α-(4-(2-hydroxyethyl)-2- n -propylphenoxy)-3,4-methylenedioxyphenylacetic acid CI-MS for C 20 H 22 O 6 : m/e = 359 (M + 1). EXAMPLE 53 N -(4- iso -propylbenzenesulfonyl)-2-(4-carbomethoxy-2- n -propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide Step A : Ethyl 2-(4-carbomethoxy-2- n -propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetate To a mixutre of methyl 4-hydroxy-3- n -propylbenzoate (3.0 g, 15.46 mmol) and Cs 2 CO 3 (5.1 g, 16 mmol) in dry dimethylformamide (50 mL) was added ethyl 2-bromo-2-(5-methoxy-3,4-methylenedioxy)phenylacetate (4.3 g, 15.56 mmol), and the resulting mixture was stirred at room temperature for 6 h. At the end of this period, the reaction mixture was diluted with ice water (300 mL) and extracted with ethyl acetate (3 x 60 mL). The combined organic phase was washed with water and brine, and then dried over anhydrous MgSO 4 , filtered and solvent removed to give the crude product. Purification of the crude product by silica-gel flash column chromatography using ethyl acetate-hexane (1:9) afforded the titled product as an oil (5.1 g). 1 H NMR (200 MHz, CDCl 3 , ppm) δ 7.82 (m, 2H); 6.75 (m, 3H); 6.61 (d, 1H, J = 1.5 Hz); 5.93 (s, 2H); 5.54 (s, 1H); 4.15 (m, 2H); 3.84 (s, 3H); 3.83 (s, 3H); 2.68 (m, 2H); 1.69 (m, 2H); 1.20 (t, 3H, J = 7.4 Hz); 0.90 (t, 3H, J = 7.4 Hz). Step B : 2-(4-carbomethoxy-2- n -propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetic acid To a solution of the product of Step A (4.3 g, 12 mmol) in methanol (25 mL) was added aqueous 2N NaOH (10 mL) and the reaction mixture was stirred at room temperature. The rapid progress of mono-deesterification was monitored by TLC analysis using CHCl 3 -MeOH-NH 4 OH:(80:15:1). After 15 min, the reaction mixture was cooled to 0°C and neutralized with aqueous 2N HCl. Methanol was removed in vacuo and the resulting mixture was acidified with aqueous 2N HCl. The oily product which precipitated was extracted into methylene chloride (3 x 40 mL) and the combined organic phase was washed with water, brine and then dried over MgSO 4 . Removal of the solvent in vacuo afforded the crude product which was then purified by flash-chromatography on silica gel using CHCl 3 -MeOH-NH 4 OH:(80:10:1) to give desired product as the ammonium salt. The salt was treated with aqueous 1N HCl (20 mL) to provide the titled compound as a white solid (3.4 g). 1 H NMR (200 MHz, CD 3 OD, ppm) δ 7.78 (m, 2H), 6.77 (m, 3H), 6.61 (d, 1H, J = 1.5 Hz), 5.93 (s, 2H), 5.54 (s, 1H), 3.84 (s, 3H), 3.83 (s, 3H), 2.68 (m, 2H), 1.69 (m, 2H), 0.90 (t, 3H, J = 7.4 Hz). Step C : N-(4- iso -Propylbenzenesulfonyl)-2-(4-carbomethoxy-2-n-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)-acetamide To the product of Step B (0.12 g, 0.30 mmol) in dry THF (1.5 mL) was added 1,1'-carbonyldiimidazole (0.1 g, 0.61 mmol) and the reaction stirred at 50°C for 3 hr. To this solution was added a solution of 4- iso -propylbenezenesulfonamide (0.17 g, 0.9 mmol) and DBU (0.14 mL, 0.94 mmol) in dry THF (1.5 mL), and the reaction continued at 50°C for 4 hr. The reaction was diluted with ice water and acidified with aqueous 1N HCl. The precipitated material was taken up in EtOAc and the organic phase was washed with water, brine, and then dried over MgSO 4 , filtered and the solvent removed. The product was purified by flash-chromatography on silica-gel using CHCl 3 :MeOH:NH 4 OH (80:10:1) as the eluting solvent to yield the titled product as the ammonium salt. Acidification of the ammonium salt afforded the titled product as a white solid (0.14 g). 1 H NMR (400 MHz, CD 3 OD, ppm): δ 7.78 (d, 2H, J = 8.4 Hz), 7.76 (d, 1H, J = 2.3 Hz), 7.62 (dd, 1H, J = 8.6, 2.2 Hz), 7.37 (d, 2H, J = 8.4 Hz), 6.70 (d, 1H, J = 1.4 Hz), 6.61 (d, 1H, J = 1.5 Hz), 5.97 (s, 2H), 5.49 (s, 1H), 3.84 (s, 3H), 3.83 (s, 3H), 2.98 (sept, 1H, J = 6.9 Hz), 2.65 (m, 2H), 1.59 (m, 2H), 1.25 (dd, 6H, J = 7.0, 2.5 Hz), 0.90 (t, 3H, J = 7.4 Hz). C 30 H 32 NO 9 N: Calc: C 59.50 H 5.33 N 2.31. Found: C 59.60 H 5.34 N 2.59 EXAMPLE 54 N-(4- iso -propylbenzenesulfonyl)-2-(4-carboxy-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide To the product of Example 53 (0.6 g, 1.02 mmol) in MeOH (15 mL) was added aqueous 2N NaOH (5 mL) and the reaction was stirred at 60°C for 3 h. When the reaction was complete the MeOH was removed in vacuo and the aqueous phase was acidified with 2N HCl. The product precipitated was extracted into methylene chloride (3 X 50 mL) and the combined organic phase was washed with brine then dried over MgSO 4 , filtered and the solvent removed. The residue upon trituration with ether provided the titled product as a white solid (0.45 g). 1 H NMR (400 MHz, DMSO-d 6 , ppm): δ 12.67 (br, 1H), 12.63 (br, 1H), 7.70 (d, 2H, J = 8.4 Hz), 7.66 (d, 1H, J = 2.1 Hz), 7.58 (dd, 1H, J = 8.5, 2.2 Hz), 7.40 (d, 2H, J = 8.4 Hz), 6.78 (d, 1H, J = 1.2 Hz), 6.66 (d, 1H, J = 1.2 Hz), 6.51 (d, 1H, J = 8.5 Hz), 6.02 (d, 2H, J = 3.1 Hz), 5.69 (s, 1H), 3.79 (s, 3H), 2.93 (sept, 1H, J = 6.9 Hz), 2.56 (m, 2H), 1.53 (m, 2H), 1.17 (d, 6H, J = 6.9 Hz), 0.83 (t, 3H, J = 7.4 Hz). FAB mass spectrum : m/e 570 (M+1). C 29 H 31 NO 9 S: Calc: C 61.15 H 5.49 N 2.46 Found: C 60.86 H 5.64 N 2.71. EXAMPLE 55 N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-(4- iso -propylbenzenesulfonyl)carboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide The titled compound was prepared from N-(4- iso -propylbenzenesulfonyl)-2-(4-carboxy-2-propylphenoxy)-5-methoxy- 3,4-methylenedioxyphenyl)acetamide (Example 54 ) using a procedure similar to that described in Step C of Example 53. FAB mass spectrum : m/e 751 (M+1). C 38 H 42 N 2 O 10 S 2 ·0.5 H 2 O: Calc.: C 60.06; H 5.70; N 3.69. Found: C 60.15; H 5.73; N 3.58. EXAMPLE 56 N-(4- iso -propylbenzenesulfonyl)-2-(4-carboxamido-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide To N-(4- iso -propylbenzenesulfonyl)-2-(4-carboxy-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide (Example 54) (0.12 g, 0.21 mmol) in dry THF (1.5 mL) was added 1,1'-carbonyldiimidazole (0.1 g, 0.61 mmol) and the mixture was stirred at 50°C for 2h. The reaction was cooled to room temperature and was saturated with dry NH 3 . The reaction mixture was stirred at room temperature for 1h and then acidified. The crude product isolated was purified by silica-gel flash column chromatography using CHCl 3 -MeOH-NH 4 OH: (40:10:1) to give the product as the ammonium salt. Acidification provided the desired titled product as a white solid (0.06 g). 1 H NMR (300 MHz, DMSO-d 6 , ppm): δ 7.76 (br, 1H), 7.68 (d, 2H, J = 8.4 Hz), 7.64 (d, 1H, J = 2.1 Hz), 7.55 (dd, 1H, J = 8.6, 2.3 Hz), 7.40 (d, 2H, J = 8.4 Hz), 7.16 (br, 1H), 6.76 (s, 1H), 6.65 (d, 1H, J = 1.2 Hz), 6.53 (d, 1H, J = 8.7 Hz), 6.01 (d, 2H, J = 2.9 Hz), 5.67 (s, 1H), 3.78 (s, 3H), 2.93 (sept, 1H, J = 6.8 Hz), 2.55 (m, 2H), 1.54 (m, 2H), 1.17 (d, 6H, J = 6.9 Hz), 0.84 (t, 3H, J = 7.3 Hz). FAB mass spectrum: m/e 569 (M+1). EXAMPLE 57 N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-methyl)carboxamido-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide The titled compound was prepared using procedures similar to those described in Example 56 1 H NMR (300 MHz, DMSO-d 6 , ppm): δ 8.21 (q, 1H, J = 4.7 Hz), 7.68 (d, 2H, J = 8.4 Hz), 7.59 (d, 1H, J = 1.9 Hz), 7.49 (dd, 1H, J = 8.6, 2.1 Hz), 7.40 (d, 2H, J = 8.4 Hz), 6.77 (s, 1H), 6.65 (s, 1H), 6.53 (d, 1H, J = 8.7 Hz), 6.01 (d, 2H, J = 2.9 Hz), 5.67 (s, 1H), 3.78 (s, 3H), 2.93 (sept, 1H, J = 6.8 Hz), 2.73 (d, 3H, J = 4.4 Hz), 2.56 (m, 2H), 1.54 (m, 2H), 1.16 (d, 6H, J = 6.9 Hz), 0.84 (t, 3H, 7.3 Hz). C 30 H 34 N 2 O 8 S: Calc: C 61.84; H 5.88; N 4.81. Found: C 61.84; H 6.03; N 4.59. EXAMPLE 58 N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-2-hydroxyethylcarboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide The titled compound was prepared using procedures similar to those described in Example 56 1 H NMR (400 MHz, CD 3 OD, ppm): δ 7.77 (d, 2H, J = 8.4 Hz), 7.64 (d, 1H, J = 2.3 Hz), 7.51 (dd, 1H, J = 8.5, 2.4 Hz), 7.36 (d, 2H, J = 8.5 Hz), 6.68 (d, 1H, J = 1.4 Hz), 6.60 (m, 2H), 5.96 (s, 2H), 5.48 (s, 1H), 3.82 (s, 3H), 3.68 (t, 2H, J = 5.9 Hz), 3.46 (t, 2H, J = 5.9 Hz), 2.97 (sept, 1H, J = 6.9 Hz), 2.66 (m, 2H), 1.62 (m, 2H), 1.25 (dd, 6H, J = 6.9, 1.2 Hz), 0.90 (t, 3H, J = 7.4 Hz). C 31 H 36 N 2 O 9 S: Calc: C 60.77; H 5.92; N 4.57. Found: C 60.49; H 6.04; N 4.45 EXAMPLE 59 N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-morpholinylcarboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide The titled compound was prepared using procedures similar to those described in Example 56. 1 H NMR (400 MHz, CD 3 OD, ppm): δ 7.77 (d, 2H, J = 8.5 Hz), 7.37 (d, 2H, J = 8.4 Hz), 7.22 (d, 1H, J = 2.1 Hz), 7.09 (dd, 1H, J = 8.4, 2.2 Hz), 6.66 (d, 1H, J = 1.5 Hz), 6.62 (d, 1H, J = 8.5 Hz), 6.57 (d, 1H, J = 1.5 Hz), 5.95 (s, 2H), 5.46 (s, 1H), 3.81 (s, 3H), 3.65 (m, 8H), 2.98 (m, 1H), 2.66 (m, 2H), 1.60 (m, 2H), 1.26 (d, 6H, J = 7.1 Hz), 0.90 (t, 3H, J = 7.4 Hz). C 33 H 38 N 2 O 9 S: Calc: C 62.05; H 6.00; N 4.39. Found: C 61.96; H 5.98; N 4.55. EXAMPLE 60 N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-3-methylbutylcarboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide The titled compound was prepared using procedures similar to those described in Example 56. 1 H NMR (400 MHz, CD 3 OD, ppm): δ 7.77 (d, 2H, J = 8.5 Hz), 7.60 (d, 1H, J = 2.3 Hz), 7.47 (dd, 1H, J = 2.3, 8.5 Hz), 7.36 (d, 2H, J = 8.5 Hz), 6.68 (d, 1H, J = 1.5 Hz), 6.59 (d, 1H, J = 1.4 Hz), 6.58 (d, 1H, J = 8.6 Hz), 5.96 (s, 2H), 5.48 (s, 1H), 3.82 (s, 3H), 3.36 (t, 2H, J = 7.5 Hz), 2.97 (m, 1H), 2.66 (m, 2H), 1.62 (m, 3H), 1.49 (q, 2H, J = 7.2 Hz), 1.25 (dd, 2H, J = 1.2, 6.9 Hz), 0.95 (d, 6H, J = 6.6 Hz), 0.90 (t, 3H, J = 7.4 Hz). C 34 H 42 N 2 O 8 S: Calc: C 63.93; H 6.63; N 4.39. Found: C 63.81; H 6.73; N 4.44. EXAMPLE 61 N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-carboxymethylcarboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide Step A : N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-t-butoxycarbonylmethylcarboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide The titled compound was prepared using procedures similar to those described in Example 56, where glycine-t-butyl ester was the amine starting material. 1 H NMR (300 MHz, CDCl 3 ppm): δ 7.70 (d, 2H, J = 8.2 Hz), 7.66 (d, 1H, J = 1.3 Hz), 7.56 (m, 1H), 7.41 (d, 2H, J = 8.2 Hz), 6.79 (s, 1H), 6.67 (s, 1H), 6.59 (d, 1H, J = 8.5 Hz), 6.03 (s, 2H), 5.71 (s, 1H), 3.88 (d, 2H, J = 5.5 Hz), 3.80 (s, 3H), 2.95 (sept, 1H, J = 6.9 Hz), 2.78 (m, 2H), 1.56 (m, 2H), 1.32 (s, 9H), 1.17 (d, 6H, J = 6.8 Hz), 0.86 (t, 3H, J = 7.3 Hz). Step B : N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-carboxymethylcarboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide A solution of the product of Step A (0.069 g, 0.1 mmol) in anhydrous trifluoroacetic acid (1.5 mL) was stirred at room temperature for 4h. The excess reagent was evaporated in vacuo and the resulting residue was triturated with dry ether to give the titled product as white solid (0.6 g). 1 H NMR (300 MHz, DMSO-d 6 , ppm): δ 7.70 (d, 2H, J = 8.2 Hz), 7.66 (d, 1H, J = 1.3 Hz), 7.56 (m, 1H), 7.41 (d, 2H, J = 8.2 Hz), 6.79 (s, 1H), 6.67 (s, 1H), 6.59 (d, 1H, J = 8.5 Hz), 6.03 (s, 2H), 5.71 (s, 1H), 3.88 (d, 2H, J = 5.5 Hz), 3.80 (s, 3H), 2.95 (sept, 1H, J = 6.9 Hz), 2.58 (m, 2H), 1.56 (m, 2H), 1.17 (d, 6H, J = 6.8 Hz), 0.86 (t, 3H, J = 7.3 Hz). C 31 H 34 N 2 O 10 S .0.4 H 2 O: Calc.: C 58.74; H 5.53; N 4.42. Found: C 58.79; H 5.83; N 4.37. EXAMPLE 62 N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-(L-Ala-OEt)carboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide The titled compound was prepared using procedures similar to those described in Example 56, where L-alanine ethyl ester was the amine starting material. 1 H NMR (400 MHz, DMSO-d 6 , ppm): δ 8.55 (d, 1H, J = 6.1 Hz), 7.69 (m, 3H), 7.57 (q, 1H, J = 9.2 Hz), 7.40 (m, 2H), 6.78 (d, 1H, J = 3.8 Hz), 6.63 (s, 1H), 6.55 (m, 1H), 6.02 (s, 2H), 5.70 (s, 1H), 4.39 (m, 1H), 4.08 (q, 2H, J = 6.8 Hz), 3.79 (d, 3H, J = 2.9 Hz), 2.93 (sept, 1H, J = 6.9 Hz), 2.57 (m, 2H), 1.55 (m, 2H), 1.37 (d, 3H, J = 5.5 Hz), 1.16 (m, 9H), 0.85 (t, 3H, J = 7.5 Hz). EXAMPLE 63 N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-2-ethoxycarbonylethylcarboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide The titled compound was prepared using procedures similar to those described in Example 56 where β-alanine ethyl ester was the amine starting material. 1 H NMR (400 MHz, DMSO-d 6 , ppm): δ 8.34 (t, 1H, J = 5.4 Hz), 7.68 (d, 2H, J = 8.3 Hz), 7.58 (d, 1H, J = 2.2 Hz), 7.49 (dd, 1H, J = 8.6, 2.3 Hz), 7.39 (d, 2H, J = 8.4 Hz), 6.77 (d, 1H, J = 1.4 Hz), 6.65 (d, 1H, J = 1.3 Hz), 6.53 (d, 1H, J = 8.8 Hz), 6.01 (s, 2H), 5.67 (s, 1H), 4.05 (q, 2H, J = 7.1 Hz), 3.78 (s, 3H), 3.44 (m, 2H), 2.92 (sept, 1H, J = 6.9 Hz), 2.53 (m, 2H), 1.54 (m, 2H), 1.16 (m, 9H), 0.84 (t, 3H, J = 7.4 Hz). EXAMPLE 64 N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-(L-Ala)carboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide The product from Example 62 was saponified to give the titled product. 1 H NMR (400 MHz, DMSO-d 6 , ppm): δ 12.64 (br, 1H), 12.51 (br, 1H), 8.44 (dd, 1H, J = 7.1, 2.7 Hz), 7.69 (m, 3H), 7.56 (m, 1H), 7.40 (m, 2H), 6.77 (d, 1H, J = 1.6 Hz), 6.66 (d, 1H, J = 1.7 Hz), 6.55 (m, 1H), 6.01 (d, 2H, J = 2.6 Hz), 5.69 (s, 1H), 4.37 (pn, 1H, J = 7.4 Hz), 3.79 (d, 3H, J = 1.9 Hz), 2.93 (sept, 1H, J = 6.9 Hz), 2.57 (m, 2H), 1.54 (m, 2H), 1.36 (dd, 3H, J = 7.3, 2.7 Hz), 1.16 (d, 6H, J = 6.8 Hz), 0.85 (t, 3H, J = 7.2 Hz). EXAMPLE 65 N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-2-carboxyethylcarboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide The product from Example 63 was saponified to give the titled product. 1 H NMR (400 MHz, DMSO-d 6 , ppm): δ 12.64 (br, 1H), 12. 21 (br, 1H), 8.32 (t, 1H, J = 5.5 Hz), 7.68 (d, 2H, J = 8.4 Hz), 7.59 (d, 1H, J = 1.9 Hz), 7.49 (dd, 1H, J = 8.5, 2.1 Hz), 7.40 (d, 2H, J = 8.4 Hz), 6.77 (s, 1H), 6.65 (d, 1H, J = 1.2 Hz), 6.01 (d, 2H, J = 2.9 Hz), 5.68 (s, 1H), 3.79 (s, 3H), 3.39 (m, 2H), 2.93 (sept, 1H, J = 6.8 Hz), 2.55 (m, 2H), 1.54 (m, 2H), 1.16 (d, 6H, J = 6.9 Hz), 0.84 (t, 3H, J = 7.3 Hz). C 32 H 36 N 2 O 10 S: Calc: C 59.99; H 5.66; N 4.37. Found: C 59.72; H 5.77; N 4.49. EXAMPLE 66 N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-3-hydroxypropylcarboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide The titled compound was prepared using procedures similar to those described in Example 56, where 3-aminopropanol was the amine starting material. 1 H NMR (400 MHz, CD 3 OD, ppm): δ 8.33 (m, 1H), 7.77 (d, 2H, J = 8.5 Hz), 7.60 (d, 1H, J = 2.3 Hz), 7.48 (dd, 1H, J = 8.5, 2.3 Hz), 7.36 (d, 2H, J = 8.4 Hz), 6.68 (d, 1H, J = 1.5 Hz), 6.60 (d, 1H, J = 1.4 Hz), 6.59 (d, 1H, J = 8.6 Hz), 5.96 (s, 2H), 5.48 (s, 1H), 3.82 (s, 3H), 3.63 (t, 2H, J = 6.3 Hz), 3.43 (t, 2H, J = 5.8 Hz), 2.97 (sept, 1H, J = 7.0 Hz), 2.66 (m, 2H), 1.80 (pn, 2H, J = 6.7 Hz), 1.61 (m, 2H), 1.25 (dd, 6H, J = 6.9, 1.3 Hz), 0.90 (t, 3H, J = 7.4 Hz). C 32 H 38 N 2 O 9 S: Calc: C 61.33; H 6.11; N 4.47. Found: C 61.07; H 6.09; N 4.48. EXAMPLE 67 N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-tetrazol-5-ylcarboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide The titled compound was prepared using procedures similar to those described in Example 56, where 5-aminotetrazole was the amine starting material. FAB-MS m/e = 640 (M+1) EXAMPLE 68 N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-3-(morpholin-4-yl)propylcarboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide The titled compound was prepared using procedures similar to those described in Example 56, where 3-(N-morpholinyl)-aminopropane was the amine starting material. 1 H NMR (400 MHz, CD 3 OD, ppm) δ 7.65 (d, 2H, J = 8.3 Hz), 7.65 (s, 1H), 7.58 (dd, 1H, J = 2.4, 8.6 Hz), 7.24 (d, 2H, J = 8.4 Hz), 6.81 (d, 1H, J = 8.6 Hz), 6.78 (d, 1H, J = 1.4 Hz), 6.69 (d, 1H, J = 1.4 Hz), 5.94 (s, 2H), 5.40 (s, 1H), 3.82 (s, 7H), 3.54 (m, 2H), 3.12 (m, 6 H), 2.92 (sept, 1H, J = 6.9 Hz), 2.66 (m, 2H), 1.62 (m, 2H), 1.22 (d, 6H, J = 6.9 Hz), 0.90 (t, 3H, J = 7.4 Hz). C 35 H 43 N 3 O 9 S .0.75 H 2 O: Calc.: C 60.46; H 6.45; N 6.04. Found: C 60.39; H 6.43; N 5.93. EXAMPLE 69 N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-(D-Ala-OMe)carboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide The titled compound was prepared using procedures similar to those described in Example 56, where D-alanine methyl ester was the amine starting material. 1 H NMR (400 MHz, CD 3 OD, ppm): δ 8.54 (d, 1H, J = 6.8 Hz); 7.77 (d, 2H, J = 8.3 Hz), 7.66 (s, 1H), 7.53 (m, 1H), 7.36 (d, 2H, J = 8.3 Hz), 6.68 (s, 1H), 6.60 (m, 2H), 5.96 (s, 2H), 5.49 (s, 1H), 4.57 (m, 1H), 3.82 (s, 3H), 3.73 (s, 3H), 2.97 (sept, 1H, J = 6.8 Hz), 2.67 (m, 2H), 1.62 (m, 2H),. 1.47 (d, 3H, J = 7.4 Hz), 1.24 (d, 6H, J = 7.0 Hz), 0.91 (t, 3H, J = 7.4 Hz). EXAMPLE 70 N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-(D-Ala)carboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide The product from Example 69 was saponified to give the titled product. 1 H NMR (400 MHz, DMSO-d 6 , ppm) δ 12.64 (br, 1H), 12.48 (br, 1H), 8.44 (dd, 1H, J = 7.3, 2.6 Hz), 7.68 (m, 3H), 7.56 (m, 1H), 7.40 (dd, 2H, J = 4.0, 8.4 Hz), 6.77 (d, 1H, J = 2.3 Hz), 6.66 (m, 1H), 6.55 (dd, 1H, J = 21.0, 8.8 Hz), 6.01 (d, 2H, J = 3.6 Hz), 5.70 (d, 1H, J = 3.8 Hz), 4.37 (pn, 1H, J = 7.3 Hz), 3.78 (d, 3H, J = 1.8 Hz), 2.93 (sept, 1H, J = 7.0 Hz), 2.57 (m, 2H), 1.55 (m, 2H), 1.36 (dd, 3H, J = 7.3, 2.7 Hz), 1.16 (d, 6H, J = 6.9 Hz), 0.85 (t, 3H, J = 7.3 Hz). EXAMPLE 71 N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-(3-carboxymethylpropyl)-carboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide The titled compound was prepared using procedures similar to those described in Example 56, where methyl γ-aminobutyrate was the amine starting material. 1 H NMR (400 MHz, CD 3 OD, ppm): δ 7.77 (d, 2H, J = 8.5 Hz), 7.61 (d, 1H, J = 2.2 Hz), 7.48 (dd, 1H, J = 8.5, 2.3 Hz), 7.36 (d, 2H, J = 8.5 Hz), 6.68 (s, 1H), 6.59 (s, 1H), 6.59 (d, 1H, J = 8.3 Hz), 5.95 (s, 2H), 5.48 (s, 1H), 4.09 (q, 2H, J = 7.1 Hz), 3.82 (s, 3H), 3.37 (m, 2H), 2.97 (sept, 1H, J = 6.9 Hz), 2.66 (m, 2H), 2.38 (t, 2H, J = 7.4 Hz), 1.89 (pn, 2H, J = 7.1 Hz), 1.61 (m, 2H), 1.23 (d, 6H, J = 6.9 Hz), 0.90 (t, 3H, J = 7.3 Hz). EXAMPLE 72 N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-(3-carboxypropyl)-carboxamido)-2- n -propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide The product from Example 71 was saponified to give the titled product. 1 H NMR (400 MHz, DMSO-d 6 , ppm): δ 12.63 (br, 1H), 12.06 (br, 1H), 8.27 (t, 1H, J = 5.5 Hz), 7.68 (d, 2H, J = 8.4 Hz), 7.60 (d, 1H, J = 2.2 Hz), 7.50 (dd, 1H, J = 8.5, 2.2 Hz), 7.40 (d, 2H, J = 8.4 Hz), 6.77 (d, 1H, J = 1.2 Hz), 6.66 (d, 1H, J = 1.3 Hz), 6.52 (d, 1H, J = 8.8 Hz), 6.01 (d, 2H, J = 2.9 Hz), 5.68 (s, 1H), 3.79 (s, 3H), 3.22 (q, 2H, J = 6.5 Hz), 2.92 (sept, 6.8 Hz), 2.54 (m, 2H), 2.25 (t, 2H, J = 7.4 Hz), 1.71 (pn, 7.1 Hz), 1.54 (m, 2H), 1.16 (d, 6H, J = 6.8 Hz), 0.84 (t, 3H, J = 7.3 Hz). C 33 H 38 N 2 O 10 S: Calc: C 60.54; H 5.85; N 4.28. Found: C 60.26; H 6.17; N 4.02. EXAMPLE 73 α-(2- n -propyl-4-methylaminosulfonylphenoxy)-3,4-methylenedioxyphenylacetic acid Step A: Preparation of 3-allyl-4-hydroxybenzenesulfonamide To a solution of 5.00 g (28.9 mmol) of 4-hydroxybenzenesulfonamide dissolved in 30 mL of anhydrous DMF was added 10.36 g (31.8 mmol) of cesium carbonate and the reaction mixture was magnetically stirred at room temperature under a nitrogen atmosphere for 10 minutes. Allyl bromide (2.75 mL, 31.8 mmol) was added and the reaction mixture was then stirred for an additional 14 hours. The reaction mixture was then partitioned between EtOAc (60 mL) and 10% aqueous citric acid (200 mL) and extracted. The organic layer was separated, washed with saturated aqueous NaHCO 3 , saturated aqueous NaCl, dried (MgSO 4 ), filtered, evaporated and dried in vacuo to afford 5.40 g (88%) of a yellow solid. The crude O -allyl ether (5.36, 25.2 mmol) was then dissolved in 10 mL of 1,2-dichlorobenzene in a 50 mL round bottom flask and magnetically stirred at reflux under a nitrogen atmosphere for 15 hours. The reaction mixture was then cooled to room temperature and diluted with methanol. The 1,2-dichlorobenzene was removed by extraction of the methanol layer with hexane, the methanol layer was separated, then evaporated. The residue was then purifed on a silica gel flash chromatography column eluted with 5% MeOH-CH 2 Cl 2 . Combination of the purified fractions, evaporation and drying in vacuo afforded 3.04 g (57%) of the title compound. 1 H-NMR (400 MHz, CD 3 OD, ppm): δ 3.38 (d, J =6.40 Hz, 2H), 5.02-5.10 (m, 2H), 5.94-6.04 (m, 1H), 6.84 (d, J =8.40 Hz, 1H), 7.58 (dd, J=2.40, 8.40 Hz, 1H), 7.61 (d, J =2.40 Hz, 1H). CI-MS m/e = 213 (M + ). Step B: Preparation of 4-hydroxy-3- n -propylbenzenesulfonamide A Parr hydrogenation flask was charged with a solution of 3.04 g (14.30 mmol) of the product of Step A dissolved in 25 mL of ethanol and 0.300 g of a 10% palladium on carbon catalyst was added. The flask was mounted in the hydrogenation apparatus, freed of air, pressurized with hydrogen (40 psig) and shaken for 15 minutes. At the end of this period TLC analysis (3% MeOH-CH 2 Cl 2 , 2 elutions) indicated that the reaction was complete and the reaction mixture was filtered and evaporated. The product was dried in vacuo to afford 3.06 g (99%) of the title compound. 1 H-NMR (400 MHz, CD 3 OD, ppm): δ 0.94 (t, J =7.20 Hz, 3H), 1.58-1.68 (m, 2H), 2.01-2.62 (m, 2H), 6.82 (d, J =8.40 Hz, 1H), 7.55 (dd, J=2.40, 8.40 Hz, 1H), 7.60 (d, J=2.40 Hz, 1H). FAB-MS m/e = 216 (M + 1). Step C: Preparation of methyl α-(2- n -propyl-4-aminosulfonylphenoxy)-3,4-methylenedioxyphenylacetate To a solution of 3.06 g (14.23 mmol) of the product of Step B dissolved in 25 mL of anhydrous DMF was added 4.87 g (15.0 mmol) of cesium carbonate and the reaction mixture was magnetically stirred under a nitrogen atmosphere at room temperature for 15 minutes. Methyl α-bromo-3,4-methylenedioxyphenylacetate (4.08g, 15.0 mmol) was then added and the reaction mixture was stirred for an additional 3 hours. The reaction mixture was then partitioned between EtOAc (80 mL) and 10% aqueous citric acid (300 mL). The organic layer was separated, washed with saturated aqueous NaHCO 3 , satuarated aqueous NaCl, dried (MgSO 4 ), filtered and evaporated. The residue was dried in vacuo to afford 5.90 g (5.79 theoretical) of the title compound which was used in the next step without further purification. 1 H-NMR (400 MHz, CD 3 OD, ppm): δ 0.97 (t, J =7.20 Hz, 3H), 1.64-1.76 (m, 2H), 2.74 (t, J =7.20 Hz, 2H), 3.70 (s, 3H), 5.87 (s, 1H), 5.97 (s, 2H), 6.85 (d, J=8.00 Hz, 1H), 6.93 (d, J=8.40 Hz, 1H), 7.03 (d, J =1.60 Hz, 1H), 7.06 (dd, J =1.60, 8.00 Hz, 1H), 7.65 (dd, J=2.40, 8.40 Hz, 1H), 7.69 (d, J=2.40 Hz, 1H). FAB-MS m/e = 408 (M + 1). Step D: Preparation of methyl α-(2- n -propyl-4-methylaminosulfonylphenoxy)-3,4-methylenedioxyphenylacetate To a solution of 2.19 g (5.38 mmol) of the product of Step C dissolved in 20 mL of anhydrous THF was added 2.41 mL (16.1 mmol) of 1,8-diazabicyclo[5.4.0]undec-7-ene and the reaction mixture was magnetically stirred under a nitrogen atmosphere for 25 minutes at room temperature. Iodomethane (1.00 mL; 16.1 mmol) was added and the reaction mixture was stirred an additional 15 hours at room temperature. The reaction mixture was diluted with EtOAc and a precipitate formed which was redissolved by addition of methanol. The mixture was further diluted with warm EtOAc (150 mL total), refridgerated overnight and a solid separated which was removed by filtration. The filtrate was evaporated in vacuo and the residue was purified on a silica gel flash chromatography column eluted with 5% EtOAc-CHCl 3 . Combination of the purified fractions and evaporation in vacuo afforded 0.164 g of the title compound and a number of impure fractions which were reserved for repurification. 1 H-NMR (400 MHz, CD 3 OD, ppm): δ 0.97 (t, J =7.20 Hz, 3H), 1.65-1.77 (m, 2H), 2.48 (s, 3H), 2.74 (t, J =7.20 Hz, 2H), 3.71 (s, 3H), 5.87 (s, 1H), 5.98 (s, 2H), 6.85 (d, J =8.00 Hz, 1H), 6.96 (d, J =8.80 Hz, 1H), 7.04 (d, J =1.60 Hz, 1H), 7.07 (dd, J=1.60, 8.00 Hz, 1H), 7.58-7.61 (m, 2H). ESI-MS m/e = 421 (M + ). Step E: Preparation of α-(2- n -propyl-4-methylaminosulfonylphenoxy)-3,4-methylenedioxyphenylacetic acid To a solution of 0.372 g (0.884 mmol) of the product of Step D dissolved in 3.0 mL of methanol was added 212 µL (1.06 mmol) of a 5.0 N aqueous sodium hydroxide solution which resulted in a cloudy suspension. The reaction was warmed to assist solution, methanol (1 mL) was added followed by dichloromethane (0.5 mL), however a clear solution was not obtained. Additional 5 N sodium hydroxide solution was added (212 µL), and finally 0.5 mL of THF was added which resulted in a clear solution. After stirring an additional 15 hours at room temperature, TLC analysis (CHCl 3 -MeOH-NH 4 OH 80:15:1) indicated complete hydrolysis of the starting material and the reaction was adjusted to pH=7 with 6 N HCl. The reaction mixture was then concentrated in vacuo and the residue was purified on a silica gel flash chromatography column eluted with CHCl 3 -MeOH-HOAc (92:7:1). Combination of the purified fractions and drying in vacuo afforded 0.335 g (93%) of the title compound as an amorphous solid. 1 H-NMR (400 MHz, CD 3 OD, ppm): δ 0.96 (t, J =7.20 Hz, 3H), 1.66-1.78 (m, 2H), 2.48 (s, 3H), 2.73-2.77 (m, 2H), 5.74 (s, 1H), 5.97 (s, 2H), 6.85 (d, J =7.60 Hz, 1H), 6.98 (d, J =9.20 Hz, 1H), 7.07-7.10 (m, 2H), 7.59-7.62 (m, 2H). ESI-MS m/e = 407 (M + ). EXAMPLE 74 N -(4- iso -propylbenzenesulfonyl)-α-(2- n -propyl-4-methylaminosulfonylphenoxy)-3,4-methylenedioxyphenylacetamide potassium salt To a solution of 0.298 g (0.73 mmol) of the product of Example 73 dissolved in 4.0 mL of anhydrous THF was added 0.237 g (1.46 mmol) of 1,1'-carbonyldiimidazole and the reaction mixture was magnetically stirred and refluxed for 2 hours under a nitrogen atmosphere. The reaction mixture was then cooled to room temperature, 0.219 g (1.10 mmol) 4- iso -propylbenzenesulfonamide and 164 µL (1.10 mmol) 1,8-diazabicyclo[5.4.0]undec-7-ene were added and the reaction was stirred and heated at reflux for an additional 10 minutes. The reaction mixture was then cooled to room temperature, partitioned between 10% aqueous citric acid and EtOAc and extracted. The organic layer which separated was washed with saturated aqueous NaCl, dried (MgSO 4 ), filtered and evaporated. The residue was redissolved in 1.0 mL of methanol and treated with 2.20 mL (3 eq) of a 1.1 M aqueous solution of potassium hydroxide. The mixture was then diluted with 5 mL of water and filtered through a 0.45 micron filter. The filtrate was desalted and purified on a Waters Millipore Delta Prep 3000 liquid chromatograph equipped with an M1000 Prep-Pak module containing a 47 x 300 mm Delta-Pak C18 15µm 100A column cartridge. Two solvent resevoirs were employed: solvent system A (95-5 water-acetonitrile), and solvent system B (5-95 water-acetonitrile), and the column effluent was monitored simultaneously at 210 and 280 nm with a Waters model 490 UV-visible detector. The column was preequillibrated with solvent system A and the filtrate was injected. The product was desalted by elution with 0.5 L of solvent system A (50 mL/min) then a gradient elution was begun which had as initial conditions 100% solvent system A-0% solvent system B and reached after 15 minutes 60% solvent system A-40% solvent system B, and the fractions were collected with an ISCO Foxy 200 fraction collector. The purified fractions were combined in round bottom flasks, frozen in a -78°C dry ice-acetone bath, and lyophilized. Combination of the purified product afforded 0.284 g (62%) of the title compound as a white lyophilized powder. 1 H-NMR (400 MHz, CD 3 OD, ppm): δ 0.89 (t, J =7.60 Hz, 3H), 1.21 (d, J =6.80 Hz, 3H), 1.22 (d, J =6.80 Hz, 3H), 1.57-1.64 (m, 2H), 2.45 (s, 3H), 2.56-2.63 (m, 1H), 2.70-2.76 (m, 1H), 5.37 (s, 1H), 5.93 (d, J =1.20 Hz, 1H), 5.94 (d, J =1.20 Hz, 1H), 6.76 (d, J =8.40 Hz, 1H), 6.85 (d, J =8.80 Hz, 1H), 7.02-7.04 (m, 2H), 7.21 (d, J =8.40 Hz, 2H), 7.47 (dd, J =2.40, 8.80 Hz, 1H), 7.52 (d, J =2.40 Hz, 1H), 7.65 (d, J =8.40 Hz, 2H). ESI-MS m/e = 627 (M + 1).

Claims: A compound of structural formula III: or a pharmaceutically acceptable salt thereof, wherein: R 3a and R 3b are independently: (a) H, (b) F, Cl, Br, or I, (c) -NO 2 , (d) (C 1 -C 6 )-alkyl, (e) -OR 7 , (f) -NHCO-(C 1 -C 4 )-alkyl, (g) -NHCO-O(C 1 -C 4 )-alkyl, (h) -O-(CH 2 )m-OR 7 , (i) -CONR 7 R 11 , or (j) -COOR 7 ; R 1 and R 2 on adjacent carbon atoms are joined together to form a ring structure: A represents: a) -Y-[C(R 6 )(R 6 )]s -Y-, or b) -C(R 4 )=C(R 5 )-C(R 4 )=C(R 5 )-; m is 2, 3 or 4, n is 0, 1 or 2, s is 1 or 2, Y is -O-, -S- and NR 7 R 4 and R 5 are independently: (a) H, (b) (C 1 -C 6 )-alkyl, (c) (C 3 -C 7 )-cycloalkyl, (d) F, Cl, Br, I, (e) -NR 7 COOR 11 , (f) -SO 2 NR 7 R 11 , (g) -O-(C 1 -C 4 )-alkyl, (h) -S(O) n -(C 1 -C 4 )-alkyl, or (i) -NHSO 2 R 11 ; R 6 is: (a) H, or (b) (C 1 -C 4 )-alkyl; R 7 is: (a) H, (b) (C 1 -C 6 )-alkyl, (c) phenyl, or (d) benzyl; R 9 and R 10 are independently: (a) H, (b) (C 1 -C 6 )-alkyl, unsubstituted or substituted with (C 3 -C 7 )-cycloalkyl, (c) Cl, Br, F, I, (d) (C 1 -C 6 )-alkoxy, or (e) hydroxy-(C 1 -C 6 )-alkyl; R 11 is (a) (C 1 -C 6 )-alkyl, unsubstituted or substituted with a substituent selected from the group consisting of: i) -OR 7 , ii) -N[R 7 ] 2 , iii) -NH 2 , iv) -COOR 7 , or v) -N[CH 2 CH 2 ] 2 Q; (b) aryl, wherein aryl is defined as phenyl or naphthyl which is unsubstituted or substituted with one or two substituents selected from the group consisting of: i) (C 1 -C 4 )-alkyl, ii) -O-(C 1 -C 4 )-alkyl, iii) -CO[NR 7 ] 2 , iv) F, Cl, Br or I, v) -COOR 7 , vi) -NH 2 , vii) -NH[(C 1 -C 4 )-alkyl], viii) -N[(C 1 -C 4 )-alkyl] 2 , or ix) -CON[CH 2 CH 2 ] 2 Q; (c) -(C 1 -C 4 )-alkylaryl, wherein aryl is as defined above, (d) (C 3 -C 7 )-cycloalkyl, (e) R 7 and R 11 on the same nitrogen atom they can join together to form a ring selected from the group consisting of: morpholinyl, piperazinyl, or pyrrolyl, or Q is O, S or -NR 7 ; R 12 is (a) H, (b) (C 1 -C 6 )-alkyl, wherein alkyl is defined as unsubstituted or substituted with one or two substituents selected from the group consisting of: i) -OH, ii) -O-(C 1 -C 4 )-alkyl, iii) -O-(C 1 -C 4 )-cycloalkyl, iv) -S(O) n -(C 1 -C 4 )-alkyl, iv) -NR 7 -(C 1 -C 4 )-alkyl, v) -NR 7 R 11 , vi) -COOR 7 , vii) -CONHR 7 , viii) -OCOR 11 , ix) -CONR 7 R 11 , x) -NR 7 CONR 7 R 11 , xi) -NR 7 COOR 11 , xii) -C(R 6 )(OH)-C(R 6 )(R 7 )(OH), or xiii) -SO 2 NR 7 R 11 , (c) -COOR 7 , (d) -CONH 2 , (e) -CONR 7 R 11 , (f) -CONR 7 CO 2 R 7 , (g) -C(R 6 )(OH)-C(R 6 )(R 7 )(OH), or (h) -CONHSO 2 R 11 , (i) -SO 2 NR 7 R 11 , (j) -NR 7 SO 2 NR 7 R 11 , (k) -CO-amino acid, wherein amino acid is defined as an L-or D- amino acid selected from the group consisting of Ala, Ile, Phe, Asp, Pro and Val and which can be further substituted as a (C 1 -C 6 )-alkyl ester or an amide, or (l) X is -O-; Z is: (a) -CO 2 H, (b) -CO 2 R 13 , (c) -CONH-(tetrazol-5-yl), (d) -CONHSO 2 -aryl, wherein aryl is defined as phenyl or naphthyl which is unsubstituted or substituted with one or two substituents selected from the group consisting of: i) (C 1 -C 4 )-alkyl, ii) -O-(C 1 -C 4 )-alkyl, iii) -CONR 7 R 11 , iv) F, Cl, Br or I, v) -COOR 7 , vi) -NH 2 , vii) -NH[(C 1 -C 4 )-alkyl], viii) -N[(C 1 -C 4 )-alkyl] 2 , or ix) -phenyl; (e) -CONHSO 2 -(C 1 -C 8 )-alkyl, wherein alkyl is unsubstituted or substituted as defined in R 4 (b), (f) -CONHSO 2 -heteroaryl, wherein heteroaryl is defined as carbazolyl, furyl, thienyl, pyrrolyl, isothiazolyl, imidazolyl, isoxazolyl, thiazolyl, oxazolyl, pyrazolyl, pyrazinyl, pyridyl, pyrimidyl, purinyl, or quinolinyl, which is unsubstituted or substituted with one or two substituents selected from the group consisting of: i) (C 1 -C 4 )-alkyl, ii) -O-(C 1 -C 4 )-alkyl, iii) -CONR 7 R 11 , iv) F, Cl, Br or I, v) -COOR 7 , vi) -NR 7 CONR 7 R 11 , and vii) -NR 7 COOR 11 ; (g) -tetrazol-5-yl; and R 13 is: (C 1 -C 4 )-alkyl. A compound according to claim 1 of structural formula IV: or a pharmaceutically acceptable salt thereof, wherein: R 1 and R 2 taken together form the ring structure: A represents: a) -Y-[C(R 6 )(R 6 )] S -Y-, or b) -C(R 4 )=C(R 5 )-C(R 4 )=C(R 5 )-; s is 1 or 2; Y is -O-; R 3a is: (a) H, (b) F, Cl, Br, or I, (c) (C 1 -C 6 )-alkyl, (d) -OR 7 , (e) -O-(CH 2 )m-OR 7 , (f) -CONR 7 R 11 , or (g) -COOR 7 ; m is 2, 3 or 4; R 4 and R 5 are independently: (a) H, (b) (C 1 -C 6 )-alkyl, (c) (C 3 -C 7 )-cycloalkyl, (d) F, Cl, Br, I, (e) -NR 7 COOR 11 , (f) -SO 2 NR 7 R 11 , (g) -O-(C 1 -C 4 )-alkyl, (h) -S(O) n -(C 1 -C 4 )-alkyl, or (i) -NHSO 2 R 11 ; n is 0, 1 or 2, R 6 is: (a) H, or (b) (C 1 -C 4 )-alkyl; R 7 is: (a) H, (b) (C 1 -C 6 )-alkyl, (c) phenyl, or (d) benzyl; R 9 is: (a) H, (b) (C 1 -C 6 )-alkyl, unsubstituted or substituted with (C 3 -C 7 )-cycloalkyl, (c) Cl, Br, F, I, (d) (C 1 -C 6 )-alkoxy, or (e) hydroxy-(C 1 -C 6 )-alkyl; R 11 is (a) (C 1 -C 6 )-alkyl, unsubstituted or substituted with a substituent selected from the group consisting of: i) -OR 7 , ii) -N[R 7 ] 2 , iii) -NH 2 , iv) -COOR 7 , or v) -N[CH 2 CH 2 ] 2 Q; (b) aryl, wherein aryl is defined as phenyl or naphthyl which is unsubstituted or substituted with one or two substituents selected from the group consisting of: i) (C 1 -C 4 )-alkyl, ii) -O-(C 1 -C 4 )-alkyl, iii) -CO[NR 7 ] 2 , iv) F, Cl, Br or I, v) -COOR 7 , vi) -NH 2 , vii) -NH[(C 1 -C 4 )-alkyl], viii) -N[(C 1 -C 4 )-alkyl] 2 , or ix) -CON[CH 2 CH 2 ] 2 Q; (c) -(C 1 -C 4 )-alkylaryl, wherein aryl is as defined above, (d) (C 3 -C 7 )-cycloalkyl, (e) R 7 and R 11 on the same nitrogen atom they can join together to form a ring selected from the group consisting of: morpholinyl, piperazinyl, or pyrrolyl, or Q is O, S or -NR 7 ; R 12 is (a) H, (b) (C 1 -C 6 )-alkyl, wherein alkyl is defined as unsubstituted or substituted with one or two substituents selected from the group consisting of: i) -OH, ii) -O-(C 1 -C 4 )-alkyl, iii) -O-(C 1 -C 4 )-cycloalkyl, iv) -S(O) n -(C 1 -C 4 )-alkyl, iv) -NR 7 -(C 1 -C 4 )-alkyl, v) -NR 7 R 11 , vi) -COOR 7 , vii) -CONHR 7 , viii) -OCOR 11 , ix) -CONR 7 R 11 , x) -NR 7 CONR 7 R 11 , xi) -NR 7 COOR 11 , xii) -C(R 6 )(OH)-C(R 6 )(R 7 )(OH), or xiii) -SO 2 NR 7 R 11 , (c) -COOR 7 , (d) -CONH 2 , (e) -CONR 7 R 11 , (f) -CONR 7 CO 2 R 7 , (g) -C(R 6 )(OH)-C(R 6 )(R 7 )(OH), or (h) -CONHSO 2 R 11 , (i) -SO 2 NR 7 R 11 , (j) -NR 7 SO 2 NR 7 R 11 , (k) -CO-amino acid, wherein amino acid is defined as an L-or D- amino acid selected from the group consisting of Ala, Ile, Phe, Asp, Pro and Val and which can be further substituted as a (C 1 -C 6 )-alkyl ester or an amide, or (l) X is (a) -O-, (b) -NR 7 -, or (c) -single bond; Z is: (a) -CO 2 H, (b) -CO 2 R 13 , (c) -CONH-(tetrazol-5-yl), (d) -CONHSO 2 -aryl, wherein aryl is defined as phenyl or naphthyl which is unsubstituted or substituted with one or two substituents selected from the group consisting of: i) (C 1 -C 4 )-alkyl, ii) -O-(C 1 -C 4 )-alkyl, iii) -CONR 7 R 11 , iv) F, Cl, Br or I, v) -COOR 7 , vi) -NH 2 , vii) -NH[(C 1 -C 4 )-alkyl], viii) -N[(C 1 -C 4 )-alkyl] 2 , or ix) -phenyl; (e) -CONHSO 2 -(C 1 -C 8 )-alkyl, wherein alkyl is unsubstituted or substituted as defined in R 4 (b), (f) -CONHSO 2 -heteroaryl, wherein heteroaryl is defined as carbazolyl, furyl, thienyl, pyrrolyl, isothiazolyl, imidazolyl, isoxazolyl, thiazolyl, oxazolyl, pyrazolyl, pyrazinyl, pyridyl, pyrimidyl, purinyl, or quinolinyl, which is unsubstituted or substituted with one or two substituents selected from the group consisting of: i) (C 1 -C 4 )-alkyl, ii) -O-(C 1 -C 4 )-alkyl, iii) -CONR 7 R 11 , iv) F, Cl, Br or I, v) -COOR 7 , vi) -NR 7 CONR 7 R 11 , and vii) -NR 7 COOR 11 , or (g) -tetrazol-5-yl; and R 13 is: (C 1 -C 4 )-alkyl. A compound according to claim 1 selected from the group consisting of: 2-[(2,6-dipropyl-4-hydroxymethyl)phenoxy]-2-(3,4-ethylenedioxyphenyl)acetic acid; 2-[(2,6-dipropyl-4-hydroxymethyl)phenoxy]-2-(3,4-methylenedioxyphenyl)acetic acid; 2-[(2,6-dipropyl-4-hydroxymethyl)phenoxy]-2-(2-naphthyl)acetic acid; 2-[(2,6-dipropyl-4-(2-hydroxyethyl)phenoxy]-2-(2-naphthyl)acetic acid; 2-[(2,6-dipropyl-4-(2-hydroxyethyl)phenoxy]-2-(3,4-methylenedioxyphenyl)acetic acid; 2-[(2,6-dipropyl-4(1,2-dihydroxyethyl)phenoxy)]-2-(2-naphthyl)acetic acid; 2-[(2,6-dipropyl-4-(1-hydroxypentyl)phenoxy]-2-(2-naphthyl)acetic acid; 2-[(4-carboxy-2,6-dipropyl)phenoxy]-2-[3,4-methylenedioxyphenyl] acetic acid; (N-4-t-butylbenzenesulfonyl)-2-(4-methoxycarbonyl-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(benzenesulfonyl)-2-(4-methoxycarbonyl-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(4-phenylbenzenesulfonyl)-2-(4-methoxycarbonyl-2-propyl-phenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(4-chlorobenzenesulfonyl)-2-(4-methoxycarbonyl-2-propyl-phenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(4-methylbenzenesulfonyl)-2-(4-methoxycarbonyl-2-propyl-phenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(5-iso-butylthien-2-ylsulfonyl)-2-(4-methoxycarbonyl-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(4-methoxybenzenesulfonyl)-2-(4-methoxycarbonyl-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(4-dimethylaminobenzenesulfonyl)-2-(4-methoxycarbonyl-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(2-methylbenzenesulfonyl)-2-(4-methoxycarbonyl-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(2-methoxycarbonylbenzenesulfonyl)-2-(4-methoxycarbonyl-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(2-chlorobenzenesulfonyl)-2-(4-methoxycarbonyl-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(3-chlorobenzenesulfonyl)-2-(4-methoxycarbonyl-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(dansylsulfonyl)-2-(4-methoxycarbonyl-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(8-quinolinesulfonyl)-2-(4-methoxycarbonyl-2-propylphenoxy)-2-(3,4-methylenedioxyphenylacetamide; N-(4-t-butylbenzenesulfonyl)-2-(4-carboxy-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(benzenesulfonyl)-2-(4-carboxy-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(4-phenylbenzenesulfonyl)-2-(4-carboxy-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(4-chlorobenzenesulfonyl)-2-(4-carboxy-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(4-methylbenzenesulfonyl)-2-(4-carboxy-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(5-isobutylthien-2-ylsulfonyl)-2-(4-carboxy-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(4-methoxybenzenesulfonyl)-2-(4-carboxy-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(4-dimethylaminobenzenesulfonyl)-2-(4-carboxy-2-propylphenoxy)-3,4-methylenedioxyphenyl)acetamide; N-(2-methylbenzenesulfonyl)-2-(4-carboxy-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(2-methoxycarbonylbenzenesulfonyl)-2-(4-carboxy-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(2-chlorobenzenesulfonyl)-2-(4-carboxy-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(3-chlorobenzenesulfonyl)-2-(4-carboxy-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; N-(dansylsulfonyl)-2-(4-carboxy-2-propylphenoxy)-3,4-methylenedioxyphenyl)acetamide; N-(8-quinolinesulfonyl)-2-(4-carboxy-2-propylphenoxy)-2-(3,4-methylenedioxyphenylacetamide; N-(8-quinolinesulfonyl)-2-(4-carboxamido-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; α-(4-carbomethoxy-2- n -propylphenoxy)-3,4-methylenedioxyphenylacetic acid; N -(4- iso -propylbenzenesulfonyl)-α-(4-carbomethoxy-2- n -propylphenoxy)-3,4-methylenedioxyphenylacetamide; N -(4- iso -propylbenzenesulfonyl)-α-(4-carboxy-2- n -propylphenoxy)-3,4-methylenedioxyphenylacetamide dipotassium salt; α-(2- iso -butyl-4-carbomethoxyphenoxy)-3,4-methylenedioxyphenylacetic acid; N -(4- iso -propylbenzenesulfonyl)-α-(2- iso -butyl-4-carbomethoxyphenoxy)-3,4-methylenedioxyphenylacetamide; N -(4- iso -propylbenzenesulfonyl)-α-(2- iso -butyl-4-carboxyphenoxy)-3,4-methylenedioxyphenylacetamide; N -(4- iso -propylbenzenesulfonyl)-α-(2- n -propyl-4-carboxamidophenoxy)-3,4-methylenedioxyphenylacetamide; N -(4- iso -propylbenzenesulfonyl)-α-(2- n -propyl-4-hydroxymethylphenoxy)-3,4-methylenedioxyphenylacetamide; α-(2- n -propylphenoxy)-3,4-methylenedioxyphenylacetic acid N -(4- iso -propylbenzenesulfonyl)-α-(2- n -propylphenoxy)-3,4-methylenedioxyphenylacetamide; α-(4-hydroxymethyl-2- n -propylphenoxy)-3,4-methylenedioxyphenylacetic acid; α-(4-(2-hydroxyethyl)-2- n -propylphenoxy)-3,4-methylenedioxyphenylacetic acid; N -(4- iso -propylbenzenesulfonyl)-2-(4-carbomethoxy-2- n -propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide; N-(4- iso -propylbenzenesulfonyl)-2-(4-carboxy-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide; N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-(4- iso -propylbenzenesulfonyl)carboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide; N-(4- iso -propylbenzenesulfonyl)-2-(4-carboxamido-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide; N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-methylcarboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide; N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-2-hydroxyethylcarboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide; N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-morpholinylcarboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide; N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-3-methylbutylcarboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide; N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-carboxymethylcarboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide; N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-(L-Ala-OEt)carboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide; N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-2-ethoxycarbonylethyl-carboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide; N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-(L-Ala)carboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide; N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-2-carboxyethylcarboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide; N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-3-hydroxypropyl-carboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide; N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-tetrazol-5-ylcarboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide; N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-3-(morpholin-4-yl)propylcarboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide; N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-(D-Ala-OMe)carboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide; N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-(D-Ala)carboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide; N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-(3-carboxymethylpropyl)carboxamido)-2-propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide; N-(4- iso -propylbenzenesulfonyl)-2-(4-(N-(3-carboxypropyl)carboxamido)-2- n -propylphenoxy)-2-(5-methoxy-3,4-methylenedioxyphenyl)acetamide; α-(2- n -propyl-4-methylaminosulfonylphenoxy)-3,4-methylenedioxyphenylacetic acid; and N -(4- iso -propylbenzenesulfonyl)-α-(2- n -propyl-4-methylaminosulfonylphenoxy)-3,4-methylenedioxyphenylacetamide potassium salt. A compound according to claim 1 selected from the group consisting of: N -(4- iso -propylbenzenesulfonyl)-α-(4-carboxy-2- n -propylphenoxy)-3,4-methylenedioxyphenylacetamide dipotassium salt; N-(8-quinolinesulfonyl)-2-(4-carboxy-2-propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide; and N-(4-dimethylaminobenzenesulfonyl)-2-(4-carboxy-2- n -propylphenoxy)-2-(3,4-methylenedioxyphenyl)acetamide, or a pharmaceutically acceptable salt. A pharmaceutical composition comprising a therapeutically effective amount of a compound as defined in any one of Claims 1 to 4 or a pharmaceutically acceptable salt thereof and a pharmaceutically acceptable carrier. A compound as defined in any one or claims 1 to 4 or a pharmaceutically acceptable salt thereof, for use in a method of treatment of the human or animal body. A compound according to Claim 6 for use in the treatment of hypertension. Use of a compound as defined in any of Claims 1 to 4 or a pharmaceutically acceptable salt thereof, for the manufacture of a medicament for the treatment of a condition selected from the group consisting of: hypertension, pulmonary hypertension, Raynaud's disease, myocardial infarction, angina pectoris, congestive heart failure, acute renal failure, cerebral infarction, cerebral vasospasm, arteriosclerosis, vascular restenosis, asthma, benign prostatic hyperplasia, inflammatory bowel diseases, endotoxic shock, endotoxin-induced multiple organ failure or disseminated intravascular coagulation, or cyclosporin-induced renal failure or hypertension in a mammal. The composition according to Claim 5 which includes another antihypertensive agent selected from: A2-adrenosine receptor agonists, α-adrenergic antagonists, angiotensin II antagonists, angiotensin converting enzyme inhibitors, β-adrenergic antagonists, atriopeptidase inhibitors(alone or with ANP), calcium channel blockers, diuretics, potassium channel agonists, renin inhibitors, sertonin antagonists, sympatholytic agents, and other antihypertensive agents, which are members selected from the group consisting of: A-69729, FK 906, FK 744, UK-73900, CSG 22492C, amiloride, atenolol, atriopeptin, bendroflumethiazide, chlorothalidone, chlorothiazide, clonidine, cromakalin, cryptenamine acetates and cryptenamine tannates, deserpidine, diazoxide, doxazosin, guanabenz, guanethidine, guanethidine sulfate, hydralazine hydrochloride, hydrochlorothiazide, isradipine, ketanserin, losartan, metolazone, metoprolol, metoprolol tartate, methyclothiazide, methyldopa, methyldopate hydrochloride, minoxidil, nadolol, pargyline hydrochloride, pinacidil, pindolol, polythiazide, prazosin, propranolol, rauwolfia serpentina , rescinnamine, reserpine, sodium nitroprusside, spironolactone, terazosin, timolol maleate, trichlormethiazide, trimethophan camsylate, verapamil, benzthiazide, quinethazone, ticrynafan, triamterene, acetazolamide, aminophylline, cyclothiazide, ethacrynic acid, furosemide, merethoxylline procaine, sodium ethacrynate, captopril, delapril hydrochloride, enalapril, enalaprilat, fosinopril sodium, lisinopril, pentopril, quinapril. quinapril hydrochloride, ramapril, teprotide, zofenopril, zofenopril calcium, diflusinal, diltiazem, felodipine, nicardipine, nifedipine, niludipine, nimodipine, nisoldipine, nitrendipine.

Inventors: BAGLEY SCOTT W, BROTEN THEODORE P, CHAKRAVARTY PRASUN K, DHANOA DALJIT S, FITCH KENNETH J, GREENLEE WILLIAM J, KEVIN NANCY JO, PETTIBONE DOUGLAS J, RIVERO RALPH A, TATA JAMES R, WALSH THOMAS F, WILLIAMS DAVID L, BAGLEY, SCOTT W., BROTEN, THEODORE P., CHAKRAVARTY, PRASUN K., DHANOA, DALJIT S., FITCH, KENNETH J., GREENLEE, WILLIAM J., KEVIN, NANCY JO, PETTIBONE, DOUGLAS J., RIVERO, RALPH A., TATA, JAMES R., WALSH, THOMAS F., WILLIAMS, DAVID L.
Applicants: MERCK & CO INC, MERCK & CO., INC.
Application year: 1994
Main classification: C07D317
IPC codes: A61P43, C07D317, A61P29, A61K31, A61P9, C07C311, C07C65, C07C59, C07D319, A61P13, C07D405, C07D257, C07D215, C07D409, A61P15, A61P11, C07D295